PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
32795895-7	2020	Overall, our study here showed the enhancement of anti-PD-1 antitumor efficacy in a syngeneic mouse model (CT-26 cells in Balb/c) by the angiogenesis inhibitor apatinib via upregulating PD-L1 expression as well as angiogenesis inhibition, which may provide a rationale for the combination of apatinib and anti-PD-1 antibody for colorectal cancer treatment in the clinic.	apatinib	160-168	programmed cell death 1	Mus musculus	310-314
33768523-9	2021	KEY RESULTS: ZE132 can effectively inhibits the PD-1/PD-L1 interactions in vitro, and it has a potent affinity to PD-L1.	ze132	13-18	programmed cell death 1	Mus musculus	48-52
33768523-12	2021	In addition, ZE132 elicits strong inhibitory effects on the mRNA expression of TGF-beta, which may serve as a potential biomarker to predict responsiveness to PD-1/PD-L1 immunotherapies.	ze132	13-18	programmed cell death 1	Mus musculus	159-163
33768523-13	2021	CONCLUSION AND IMPLICATIONS: We identified a new lead compound ZE132 targeting PD-1/PD-L1 interactions, not only showing favorable drug-like properties in vitro and in vivo, but also showing the advantage of overcoming the barrier of TIME compared to anti-PD-1 antibody.	ze132	63-68	programmed cell death 1	Mus musculus	79-83
33768523-13	2021	CONCLUSION AND IMPLICATIONS: We identified a new lead compound ZE132 targeting PD-1/PD-L1 interactions, not only showing favorable drug-like properties in vitro and in vivo, but also showing the advantage of overcoming the barrier of TIME compared to anti-PD-1 antibody.	ze132	63-68	programmed cell death 1	Mus musculus	256-260
33233585-5	2020	Here, we confirm that the oscillatory behaviour of the response biomarker is also detected in mice treated with anti PD-1 immunotherapy both in combination with temozolomide and as monotherapy.	Temozolomide	161-173	programmed cell death 1	Mus musculus	117-121
32795895-0	2020	Apatinib enhanced anti-PD-1 therapy for colon cancer in mice via promoting PD-L1 expression.	apatinib	0-8	programmed cell death 1	Mus musculus	23-27
32795895-2	2020	In this study, we found that an angiogenesis inhibitor apatinib enhanced anti-PD-1 therapy for colon cancer in mice via promoting PD-L1 expression.	apatinib	55-63	programmed cell death 1	Mus musculus	78-82
32795895-7	2020	Overall, our study here showed the enhancement of anti-PD-1 antitumor efficacy in a syngeneic mouse model (CT-26 cells in Balb/c) by the angiogenesis inhibitor apatinib via upregulating PD-L1 expression as well as angiogenesis inhibition, which may provide a rationale for the combination of apatinib and anti-PD-1 antibody for colorectal cancer treatment in the clinic.	apatinib	292-300	programmed cell death 1	Mus musculus	55-59
32795895-4	2020	Further, apatinib-treated cancer cells hampered activation and IFN-gamma secretion of T cells in the co-culture system, which was reversed by the anti-PD-1 antibody.	apatinib	9-17	programmed cell death 1	Mus musculus	151-155
32795895-7	2020	Overall, our study here showed the enhancement of anti-PD-1 antitumor efficacy in a syngeneic mouse model (CT-26 cells in Balb/c) by the angiogenesis inhibitor apatinib via upregulating PD-L1 expression as well as angiogenesis inhibition, which may provide a rationale for the combination of apatinib and anti-PD-1 antibody for colorectal cancer treatment in the clinic.	apatinib	160-168	programmed cell death 1	Mus musculus	55-59
34898004-8	2022	More importantly, Carfilzomib synergized with PD-1 antibody to almost completely regress autochthonous lung cancers.	carfilzomib	18-29	programmed cell death 1	Mus musculus	46-50
34160685-8	2022	ICB therapy of anti-PD-1/anti-CTLA-4 antibodies promoted T-cell infiltration into tumor tissues, whereas no definite antitumor effect was observed.	indole-2-carboxylic acid	0-3	programmed cell death 1	Mus musculus	20-24
34987517-9	2021	More importantly, combination with sirolimus and anti-PD-1 synergistically inhibits tumor growth via inducing the immunogenic cell death of tumor cells in vivo.	Sirolimus	35-44	programmed cell death 1	Mus musculus	54-58
34450250-7	2022	GDNPs enhanced PD-1 mAb anti-tumor efficacy in activating tumor infiltrated T lymphocytes.	gdnps	0-5	programmed cell death 1	Mus musculus	15-19
34450250-9	2022	In situ activation of TAMs by GDNPs may broadly serve as a facile platform to modulate the suppressive cold-TME and optimize the PD-1 mAb immunotherapy in future clinical application.	tams	22-26	programmed cell death 1	Mus musculus	129-133
34727389-5	2022	CPI-203, a small-molecule bromodomain-containing protein 4 (BRD4) inhibitor, which can potently inhibit the PD-L1 expression in vitro and vivo, combined with PD-1 antibody improved the response to immunotherapy in a liver cancer model.	CPI203	0-7	programmed cell death 1	Mus musculus	158-162
34675118-7	2022	We demonstrate that TP-0903 as a single agent or in combination with gemcitabine and/or anti-programmed cell death protein 1 (PD1) antibody has anti-metastatic and anti-tumor effects in PDA tumor bearing mice, leading to increased survival.	dubermatinib	20-27	programmed cell death 1	Mus musculus	93-124
34675118-7	2022	We demonstrate that TP-0903 as a single agent or in combination with gemcitabine and/or anti-programmed cell death protein 1 (PD1) antibody has anti-metastatic and anti-tumor effects in PDA tumor bearing mice, leading to increased survival.	dubermatinib	20-27	programmed cell death 1	Mus musculus	126-129
34675118-9	2022	This effect was augmented when TP-0903 was combined with gemcitabine and anti-PD1 antibody.	dubermatinib	31-38	programmed cell death 1	Mus musculus	78-81
34698902-9	2022	DHA-dFdC enabled Panc-02 tumors to respond to anti-PD-1 mAb.	dha-dfdc	0-8	programmed cell death 1	Mus musculus	51-55
34698902-11	2022	CONCLUSION: DHA-dFdC is a bona fide ICD inducer and can render pancreatic tumors responsive to anti-PD-1 mAb therapy.	dha-dfdc	12-20	programmed cell death 1	Mus musculus	100-104
34515617-0	2021	Combination immunotherapy of chlorogenic acid liposomes modified with sialic acid and PD-1 blockers effectively enhances the anti-tumor immune response and therapeutic effects.	Chlorogenic Acid	29-45	programmed cell death 1	Mus musculus	86-90
34774620-8	2021	Ectopic expression of SARI induces cancer-specific cell death in human OSCC cell lines and in a paclitaxel plus cisplatin non-responder OSCC patient-derived (PDC1) cell line.	Paclitaxel	96-106	programmed cell death 1	Mus musculus	158-162
34774620-10	2021	Using a nude mouse xenograft model, we show that intratumoral injections of Ad.SARI significantly reduce PDC1 tumor burden, whereas treatment with an ER stress inhibitor efficiently rescues tumors from growth inhibition.	ad	76-78	programmed cell death 1	Mus musculus	105-109
34872935-0	2022	Sequential administration of pemetrexed and cisplatin reprograms tumor immune microenvironment and potentiates PD-1/PD-L1 treatment in a lung cancer model.	Pemetrexed	29-39	programmed cell death 1	Mus musculus	111-115
34872935-0	2022	Sequential administration of pemetrexed and cisplatin reprograms tumor immune microenvironment and potentiates PD-1/PD-L1 treatment in a lung cancer model.	Cisplatin	44-53	programmed cell death 1	Mus musculus	111-115
34515617-11	2021	CA-SAL and anti-PD1 Ab combination therapy presented synergistic anti-tumor activity, which enhanced the efficacy of the PD-1 checkpoint blocker in a mouse model of melanoma.	ca-sal	0-6	programmed cell death 1	Mus musculus	121-125
34887262-11	2021	SN-38 or metformin sensitized unresponsive tumors responding to anti-PD-1 therapy by engaging NK or CD8+ T cells to infiltrate the tumor microenvironment (TME) and secret interferon-gamma and granzyme B to kill tumors.	Irinotecan	0-5	programmed cell death 1	Mus musculus	69-73
34571082-6	2021	Taken together, these results demonstrate that statins, administered in combination with anti-PD-1 antibody, could enhance the anticancer effect of cisplatin and potentiate the efficacy of immunotherapy for HNSCC and present a rationale for repurposing statins as an adjuvant immunotherapeutic option for HNSCC.	Cisplatin	148-157	programmed cell death 1	Mus musculus	94-98
34887262-11	2021	SN-38 or metformin sensitized unresponsive tumors responding to anti-PD-1 therapy by engaging NK or CD8+ T cells to infiltrate the tumor microenvironment (TME) and secret interferon-gamma and granzyme B to kill tumors.	Metformin	9-18	programmed cell death 1	Mus musculus	69-73
34912335-4	2021	In the PD-1cKO mice, a complete deletion of Pdcd1 in tumor-infiltrating T cells (TILs) after tamoxifen treatment led to the inhibition of tumor growth of both small and large tumors.	Tamoxifen	93-102	programmed cell death 1	Mus musculus	44-49
34761679-0	2021	Design, Synthesis, and Pharmacological Evaluation of Biaryl-Containing PD-1/PD-L1 Interaction Inhibitors Bearing a Unique Difluoromethyleneoxy Linkage.	Biaryl	53-59	programmed cell death 1	Mus musculus	71-75
34900690-0	2021	Alphataxin, a Small-Molecule Drug That Elevates Tumor-Infiltrating CD4+ T Cells, in Combination With Anti-PD-1 Therapy, Suppresses Murine Renal Cancer and Metastasis.	alphataxin	0-10	programmed cell death 1	Mus musculus	106-110
34607937-9	2021	In addition, we found in vitro and in vivo that Tregs in the presence of anti-PD-1 proliferated more than control Tregs PD-1 blockade significantly increased the suppressive activity of Tregs at biologically relevant Treg/Tnaive cell ratios.	tregs	48-53	programmed cell death 1	Mus musculus	78-82
34900690-13	2021	Orally available Alphataxin, the first and only drug developed to increase CD4+ T cells, in combination with anti-PD-1, is a powerful therapeutic method that provides long-term remission in renal cell carcinoma and potentially other T cell-responsive cancers by increasing the number of CD4+ tumor-infiltrating T cells.	alphataxin	17-27	programmed cell death 1	Mus musculus	114-118
34815361-8	2022	We show for the first time that potent cyclic dinucleotides can promote a rapid and stronger induction of the same genes eventually regulated by PD-1 blockade.	cyclic dinucleotides	39-59	programmed cell death 1	Mus musculus	145-149
34607937-7	2021	Based on these data, we hypothesized that anti-PD-1 treatment on Tregs results in a prosurvival phenotype.	tregs	65-70	programmed cell death 1	Mus musculus	47-51
34838121-13	2021	We discovered that cell-specific CD39 expression in macrophages and CD73 expression in HCC cells synergistically activated the eATP-adenosine pathway and produced more adenosine, thereby impairing CD8+ T cell function and driving anti-PD1 resistance.	Adenosine	132-141	programmed cell death 1	Mus musculus	235-238
34838121-13	2021	We discovered that cell-specific CD39 expression in macrophages and CD73 expression in HCC cells synergistically activated the eATP-adenosine pathway and produced more adenosine, thereby impairing CD8+ T cell function and driving anti-PD1 resistance.	Adenosine	168-177	programmed cell death 1	Mus musculus	235-238
34607937-9	2021	In addition, we found in vitro and in vivo that Tregs in the presence of anti-PD-1 proliferated more than control Tregs PD-1 blockade significantly increased the suppressive activity of Tregs at biologically relevant Treg/Tnaive cell ratios.	tregs	48-53	programmed cell death 1	Mus musculus	120-124
34607937-8	2021	Indeed, Tregs exposed to PD-1 blockade had significantly higher levels of Bcl-2 expression, and this led to increased protection from glucocorticoid-induced apoptosis.	tregs	8-13	programmed cell death 1	Mus musculus	25-29
34607937-9	2021	In addition, we found in vitro and in vivo that Tregs in the presence of anti-PD-1 proliferated more than control Tregs PD-1 blockade significantly increased the suppressive activity of Tregs at biologically relevant Treg/Tnaive cell ratios.	tregs	186-191	programmed cell death 1	Mus musculus	78-82
34607937-9	2021	In addition, we found in vitro and in vivo that Tregs in the presence of anti-PD-1 proliferated more than control Tregs PD-1 blockade significantly increased the suppressive activity of Tregs at biologically relevant Treg/Tnaive cell ratios.	tregs	186-191	programmed cell death 1	Mus musculus	120-124
34737267-4	2021	In CT26 and MC38 syngeneic mouse tumour models, IBI319 restricts T cell co-stimulation to PD-1-rich microenvironments, such as tumours and tumour-draining lymph nodes, hence systemic (liver) toxicity arising from generalised T cell activation is reduced.	ibi319	48-54	programmed cell death 1	Mus musculus	90-94
34753889-8	2021	Monotherapy of a B16-F10 mouse model with anti-PD-1 resulted in a moderate therapeutic effect that could be enhanced by entinostat.	entinostat	120-130	programmed cell death 1	Mus musculus	47-51
34737267-5	2021	Besides limiting systemic T cell co-stimulation, the anti-PD-1 arm of IBI319 also exhibits checkpoint blockade functions, with an overall result of T and NK cell infiltration into tumours.	ibi319	70-76	programmed cell death 1	Mus musculus	58-62
34242713-4	2021	METHODS: Female 129Sv/Ev mice were inoculated with 344SQ anti-PD1-resistant (344SQR) or anti-PD1-sensitive (344SQP) metastatic lung cancer cells in the right leg on day 0 ("primary" tumor) and the left leg on day 4 ("secondary" tumor).	344sq	51-56	programmed cell death 1	Mus musculus	62-65
34560814-0	2021	Quercetin inhibiting the PD-1/PD-L1 interaction for immune-enhancing cancer chemopreventive agent.	Quercetin	0-9	programmed cell death 1	Mus musculus	25-29
34824160-7	2021	RESULTS: The addition of BEMPEG or anti-CTLA-4 to the combination of vaccine and anti-PD-1 led to complete eradication of large tumors in nearby 100% of treated animals, in association with expansion and activation of cancer neoantigen-specific T cells and reduction of tumor-infiltrating Tregs.	bempeg	25-31	programmed cell death 1	Mus musculus	86-90
34841231-7	2021	DOX also inhibited tumor growth and enhanced the antitumor activity of PD-1 inhibitors in C57BL6 and BALB/c mice subcutaneously inoculated with B16-F10 and 4T1 cells, respectively.	Doxycycline	0-3	programmed cell death 1	Mus musculus	71-75
34841231-8	2021	In conclusion, the combination of DOX and PD-1 inhibitor could be an anticancer strategy.	Doxycycline	34-37	programmed cell death 1	Mus musculus	42-46
34815353-10	2021	However, we observed an increased number of CD8 T cells expressing PD-1, Ki-67, Tim-3, and CD62L as well as increased effector cytokine production after treatment with metformin and tumor membrane vesicle vaccine.	Metformin	168-177	programmed cell death 1	Mus musculus	67-71
34560814-3	2021	Here we report that quercetin dihydrate was screened and shown to inhibit the PD-1/PD-L1 interaction.	Quercetin dihydrate	20-39	programmed cell death 1	Mus musculus	78-82
34560814-7	2021	These results suggest that quercetin dihydrate attenuates the inhibitory effect of PD-L1 on T cells by inhibiting the PD-1/PD-L1 interaction, which has an exciting potential to be used as a cancer chemopreventive agent.	Quercetin dihydrate	27-46	programmed cell death 1	Mus musculus	118-122
34160137-5	2021	Also, NE-LMP facilitates CTL infiltration in tumors and exhibits enhanced chemo-immunotherapy in combination of PD-1 immune checkpoint blockade treatment in orthotopic 4T1 tumor-bearing mice, with significantly prolonged survival.	ne-lmp	6-12	programmed cell death 1	Mus musculus	112-116
34712512-5	2021	We find that Vgamma2Vdelta2 T cells express PD-1, CTLA-4, LAG-3, and TIM-3 inhibitory receptors during the 14-day ex vivo expansion period, and PD-1, LAG-3, and TIM-3 upon subsequent stimulation by pamidronate-treated tumor cells.	Pamidronate	198-209	programmed cell death 1	Mus musculus	144-148
34622729-7	2021	RESULTS: In mice administered piceatannol (12.5 mg/kg), the tumor number, tumor area, and Ki-67-positive cell numbers decreased by 30.1%, 57.2%, and 89.1%, respectively, colon MCP-1 and PD-1 levels showed reductions of 43.8% and 70.9%, respectively, and COX-2-positive cell numbers declined by 60.2%.	3,3',4,5'-tetrahydroxystilbene	30-41	programmed cell death 1	Mus musculus	186-190
34622729-8	2021	CONCLUSIONS: The inhibitory effects of piceatannol on AOM/DSS-induced colon tumor growth appear to be associated with reductions in colon MCP-1 and PD-1 levels through the downregulated expression of COX-2 in the tumor microenvironment.	3,3',4,5'-tetrahydroxystilbene	39-50	programmed cell death 1	Mus musculus	148-152
34622729-8	2021	CONCLUSIONS: The inhibitory effects of piceatannol on AOM/DSS-induced colon tumor growth appear to be associated with reductions in colon MCP-1 and PD-1 levels through the downregulated expression of COX-2 in the tumor microenvironment.	Azoxymethane	54-57	programmed cell death 1	Mus musculus	148-152
34622729-8	2021	CONCLUSIONS: The inhibitory effects of piceatannol on AOM/DSS-induced colon tumor growth appear to be associated with reductions in colon MCP-1 and PD-1 levels through the downregulated expression of COX-2 in the tumor microenvironment.	Dextran Sulfate	58-61	programmed cell death 1	Mus musculus	148-152
34638488-7	2021	Moreover, the combination of MSU42011 and immunotherapy (anti-PDL1 and anti-PD1 antibodies) significantly (p < 0.05) reduced tumor size vs. individual treatments.	msu42011	29-37	programmed cell death 1	Mus musculus	76-79
34536044-6	2021	Anti-PD-1 antibody and metformin can improve the efficacy of nanovaccines.	nanovaccines	61-73	programmed cell death 1	Mus musculus	5-9
34622984-9	2022	In summary, SHED-mediated rescue of Treg/Th17 balance via the sPD-L1/PD-1 pathway ameliorates the gland inflammation and dryness symptoms in SS mice.	treg	36-40	programmed cell death 1	Mus musculus	69-73
34265852-2	2021	Although inhibition of mTOR signaling promotes tumor cell death and several mTOR inhibitors have been used clinically, recent reports have shown that co-treatment with MHY1485, an mTOR activator, enhances the anti-cancer effects of anti-PD-1 antibody and 5-fluorouracil.	4,6-dimorpholino-N-(4-nitrophenyl)-1,3,5-triazin-2-amine	168-175	programmed cell death 1	Mus musculus	237-241
34600560-3	2021	The present study exploits atovaquone/albumin nanoparticles to improve bioavailability and tumor targeting of atovaquone, enhancing the efficacy of anti-PD-1 therapy by normalizing tumor hypoxia.	Atovaquone	27-37	programmed cell death 1	Mus musculus	153-157
34600560-3	2021	The present study exploits atovaquone/albumin nanoparticles to improve bioavailability and tumor targeting of atovaquone, enhancing the efficacy of anti-PD-1 therapy by normalizing tumor hypoxia.	Atovaquone	110-120	programmed cell death 1	Mus musculus	153-157
34600560-11	2021	When combined with anti-PD-1 antibody, we observed that HSA-ATO NPs strongly enhanced the response of mice bearing tumor xenografts to immunotherapy.	hsa-ato	56-63	programmed cell death 1	Mus musculus	24-28
34572136-2	2021	In multiple mouse cancer models, de novo synthesis of mevalonate and cholesterol inhibitors was found to synergize with anti-PD-1 antibody therapy.	Mevalonic Acid	54-64	programmed cell death 1	Mus musculus	125-129
34481337-0	2021	Discovery of 1,3,4-oxadiazole derivatives as potential antitumor agents inhibiting the programmed cell death-1/programmed cell death-ligand 1 interaction.	1,3,4-oxadiazole	13-29	programmed cell death 1	Mus musculus	87-141
34478928-1	2021	Here we report a novel combination of a caspase-cleavable peptide-doxorubicin conjugate (MPD-1) with CD47-antagonizing nanocage therapeutics for the treatment of microsatellite-stable (MSS) colorectal cancer (CRC).	Doxorubicin	66-77	programmed cell death 1	Mus musculus	89-94
34478928-2	2021	MPD-1 (i) upregulated markers of immunogenic cell death (ICD) in tumor, and increased co-stimulatory markers on dendritic cells (DCs), (ii) enhanced CD8+ T cell infiltration and antigen presenting cell (APC) activation, and (iii) showed negligible off-target immune-related toxicity compared to free dox.	Doxorubicin	300-303	programmed cell death 1	Mus musculus	0-5
34517894-0	2021	Regorafenib enhances anti-PD1 immunotherapy efficacy in murine colorectal cancers and their combination prevents tumor regrowth.	regorafenib	0-11	programmed cell death 1	Mus musculus	26-29
34196474-5	2021	Immune checkpoint inhibitor (Anti-PD-1 antibody) is trapped in the interior of the porous ZGO@TiO2 with paclitaxel (PTX) loaded liposome encapsulation to form ZGO@TiO2 @ALP.	zgo	90-93	programmed cell death 1	Mus musculus	34-38
34196474-5	2021	Immune checkpoint inhibitor (Anti-PD-1 antibody) is trapped in the interior of the porous ZGO@TiO2 with paclitaxel (PTX) loaded liposome encapsulation to form ZGO@TiO2 @ALP.	titanium dioxide	94-98	programmed cell death 1	Mus musculus	34-38
34196474-5	2021	Immune checkpoint inhibitor (Anti-PD-1 antibody) is trapped in the interior of the porous ZGO@TiO2 with paclitaxel (PTX) loaded liposome encapsulation to form ZGO@TiO2 @ALP.	Paclitaxel	104-114	programmed cell death 1	Mus musculus	34-38
34196474-5	2021	Immune checkpoint inhibitor (Anti-PD-1 antibody) is trapped in the interior of the porous ZGO@TiO2 with paclitaxel (PTX) loaded liposome encapsulation to form ZGO@TiO2 @ALP.	Paclitaxel	116-119	programmed cell death 1	Mus musculus	34-38
34196474-5	2021	Immune checkpoint inhibitor (Anti-PD-1 antibody) is trapped in the interior of the porous ZGO@TiO2 with paclitaxel (PTX) loaded liposome encapsulation to form ZGO@TiO2 @ALP.	zgo	159-162	programmed cell death 1	Mus musculus	34-38
34196474-5	2021	Immune checkpoint inhibitor (Anti-PD-1 antibody) is trapped in the interior of the porous ZGO@TiO2 with paclitaxel (PTX) loaded liposome encapsulation to form ZGO@TiO2 @ALP.	titanium dioxide	163-167	programmed cell death 1	Mus musculus	34-38
34196474-7	2021	After intravenous injection, ultrasound irradiation at GBM sites initiates ROS generation from ZGO@TiO2 @ALP, leading to liposome destruction for PTX and anti-PD-1 antibody release to kill tumors and induce local inflammation, which in-turn attractes more ZGO@TiO2 @ALP-NEs to migrate into tumor sites for augmented and sustained therapy.	Reactive Oxygen Species	75-78	programmed cell death 1	Mus musculus	159-163
34196474-7	2021	After intravenous injection, ultrasound irradiation at GBM sites initiates ROS generation from ZGO@TiO2 @ALP, leading to liposome destruction for PTX and anti-PD-1 antibody release to kill tumors and induce local inflammation, which in-turn attractes more ZGO@TiO2 @ALP-NEs to migrate into tumor sites for augmented and sustained therapy.	zgo	95-98	programmed cell death 1	Mus musculus	159-163
34196474-7	2021	After intravenous injection, ultrasound irradiation at GBM sites initiates ROS generation from ZGO@TiO2 @ALP, leading to liposome destruction for PTX and anti-PD-1 antibody release to kill tumors and induce local inflammation, which in-turn attractes more ZGO@TiO2 @ALP-NEs to migrate into tumor sites for augmented and sustained therapy.	titanium dioxide	99-103	programmed cell death 1	Mus musculus	159-163
34196474-7	2021	After intravenous injection, ultrasound irradiation at GBM sites initiates ROS generation from ZGO@TiO2 @ALP, leading to liposome destruction for PTX and anti-PD-1 antibody release to kill tumors and induce local inflammation, which in-turn attractes more ZGO@TiO2 @ALP-NEs to migrate into tumor sites for augmented and sustained therapy.	zgo	256-259	programmed cell death 1	Mus musculus	159-163
34196474-7	2021	After intravenous injection, ultrasound irradiation at GBM sites initiates ROS generation from ZGO@TiO2 @ALP, leading to liposome destruction for PTX and anti-PD-1 antibody release to kill tumors and induce local inflammation, which in-turn attractes more ZGO@TiO2 @ALP-NEs to migrate into tumor sites for augmented and sustained therapy.	titanium dioxide	260-264	programmed cell death 1	Mus musculus	159-163
34342231-5	2021	Moreover, phloridzin augmented the number of CD8+CD122+PD-1+ Tregs and CD4+FoxP3+ Tregs in HFD-fed C57BL/6J mice and HFD-fed aP2-SREBF1c mice and downregulated the mTORC1/SREBP-1c signaling pathway-related protein expressions in vivo and in vitro.	Phlorhizin	10-20	programmed cell death 1	Mus musculus	55-59
34466002-10	2021	The increase of adenosine in tumor tissue by anti-PD-1 mAb alone was suppressed by SHR170008 in the combination groups.	Adenosine	16-25	programmed cell death 1	Mus musculus	50-54
34466002-12	2021	Conclusion: Our findings suggest that CD73 may serve as an immune checkpoint by generating adenosine, which suppresses the antitumor activity of anti-PD-1 mAb, and inhibition of CD73 may be a potential beneficial combination partner with immune-checkpoint inhibitors to improve their therapeutic outcomes in general.	Adenosine	91-100	programmed cell death 1	Mus musculus	150-154
34479922-9	2021	Remarkably, intratumoral IMO-2125 in combination with systemic anti-PD1 causes a potent antitumor effect on primary injected and distant sites also in pancreatic cancer models with low immunogenic potential, preceded by a transition toward an immunopermissive microenvironment, with increase in tumor-infiltrating dendritic and T cells in tumor and lymph nodes.	imo-2125	25-33	programmed cell death 1	Mus musculus	68-71
34229208-5	2021	Thus, in contrast to other tumors, Tregs did not become dysfunctional despite chronic stimulation in the tumor microenvironment and progressive up-regulation of PD-1.	tregs	35-40	programmed cell death 1	Mus musculus	161-165
34466002-1	2021	Introduction: CD73 and adenosine support growth-promoting neovascularization, metastasis, and survival in cells, and promote anti-PD-1 mAb therapy-induced immune escape.	Adenosine	23-32	programmed cell death 1	Mus musculus	130-134
34429969-6	2021	Results: The injection of caerin 1.1/1.9 increased the efficacy of vaccinated TC-1 tumor-bearing mice with anti-PD-1 treatment and largely expanded the populations of macrophages and NK cells with higher immune activation level, while reducing immunosuppressive macrophages.	caerin	26-32	programmed cell death 1	Mus musculus	112-116
34290705-0	2021	Total Glucosides of Paeony Ameliorate Pristane-Induced Lupus Nephritis by Inducing PD-1 ligands+ Macrophages via Activating IL-4/STAT6/PD-L2 Signaling.	Glucosides	6-16	programmed cell death 1	Mus musculus	83-87
34388730-14	2022	CONCLUSIONS: In this study, the authors showed synergy between anti-PD-1 immunotherapy and glutamate modulation.	Glutamic Acid	91-100	programmed cell death 1	Mus musculus	68-72
34174350-3	2021	Here, we describe cRGD-functionalized chimaeric polymersomes (cRGD-CPs) as a robust systemic delivery vehicle for LTX-315, which in combination with CpG adjuvant and anti-PD-1 boost immunotherapy of malignant B16F10 melanoma in mice.	LTX-315	114-121	programmed cell death 1	Mus musculus	171-175
34451932-8	2021	Therefore, RD of an anti-PD-1 CPI therapy for CRCLM may improve the therapeutic index by reducing the total dose required and limiting the systemic exposure.	methyl 2-isocyano-2-methylpropanoate	30-33	programmed cell death 1	Mus musculus	25-29
34290904-7	2021	Results: Mice implanted with PCL:PEG:PCL hydrogels carrying anti-PD-1 at the site of their lymph nodes showed significantly improved survival outcomes compared to mice systemically treated with anti-PD-1 (P = .0185).	Polyethylene Glycols	33-36	programmed cell death 1	Mus musculus	65-69
34196308-5	2021	Inhibition of the IFN response pathway using the JAK1/JAK2 inhibitor ruxolitinib decreased PD-L1 expression on myeloid-derived suppressor cells in the brain and further potentiated the therapeutic effect of MV-s-NAP-uPA and anti-PD1.	ruxolitinib	69-80	programmed cell death 1	Mus musculus	229-232
34290705-0	2021	Total Glucosides of Paeony Ameliorate Pristane-Induced Lupus Nephritis by Inducing PD-1 ligands+ Macrophages via Activating IL-4/STAT6/PD-L2 Signaling.	pristane	38-46	programmed cell death 1	Mus musculus	83-87
34188068-5	2021	In combination, YIV-906 reduced PD1 or counteracted PD-L1 induction caused by anti-PD1 which led to higher T-cell activation gene expression of the tumor.	yiv-906	16-23	programmed cell death 1	Mus musculus	32-35
34249005-10	2021	These proliferative alloreactive T-cells expressed greater levels of PD-1 and underwent increased programmed cell death as the concentration of BEN exposure increased.	Bendamustine Hydrochloride	144-147	programmed cell death 1	Mus musculus	69-73
34326168-0	2021	Tryptophan potentiates CD8+ T cells against cancer cells by TRIP12 tryptophanylation and surface PD-1 downregulation.	Tryptophan	0-10	programmed cell death 1	Mus musculus	97-101
34326168-4	2021	The effect of tryptophan and IDO inhibitors on cell surface programmed cell death protein 1 (PD-1) level were measured by flow cytometry.	Tryptophan	14-24	programmed cell death 1	Mus musculus	60-91
34326168-4	2021	The effect of tryptophan and IDO inhibitors on cell surface programmed cell death protein 1 (PD-1) level were measured by flow cytometry.	Tryptophan	14-24	programmed cell death 1	Mus musculus	93-97
34326168-7	2021	RESULTS: Here, we reported that IDO inhibitors activated CD8+ T cells also by accumulating tryptophan that downregulated PD-1.	Tryptophan	91-101	programmed cell death 1	Mus musculus	121-125
34326168-8	2021	Tryptophan and IDO inhibitors administration, both increased intracellular tryptophan, and tryptophanyl-tRNA synthetase (WARS) overexpression decreased Jurkat and mice CD8+ T cell surface PD-1.	Tryptophan	0-10	programmed cell death 1	Mus musculus	188-192
34326168-10	2021	SIRT1 de-tryptophanylated TRIP12 and reversed the effects of tryptophan and WARS on PD-1.	Tryptophan	61-71	programmed cell death 1	Mus musculus	84-88
34326168-12	2021	CONCLUSIONS: Our results revealed the immune-activating efficacy of tryptophan, and suggested tryptophan supplemental may benefit IDO inhibitors and PD-1 blockade during anticancer treatments.	Tryptophan	68-78	programmed cell death 1	Mus musculus	149-153
34326168-12	2021	CONCLUSIONS: Our results revealed the immune-activating efficacy of tryptophan, and suggested tryptophan supplemental may benefit IDO inhibitors and PD-1 blockade during anticancer treatments.	Tryptophan	94-104	programmed cell death 1	Mus musculus	149-153
34188068-5	2021	In combination, YIV-906 reduced PD1 or counteracted PD-L1 induction caused by anti-PD1 which led to higher T-cell activation gene expression of the tumor.	yiv-906	16-23	programmed cell death 1	Mus musculus	83-86
34078817-0	2021	Increasing Tumor Extracellular pH by an Oral Alkalinizing Agent Improves Antitumor Responses of Anti-PD-1 Antibody: Implication of Relationships between Serum Bicarbonate Concentrations, Urinary pH, and Therapeutic Outcomes.	Bicarbonates	159-170	programmed cell death 1	Mus musculus	101-105
34094037-9	2021	Doxorubicin also suppressed significantly (P<0.05) the relative expression of PD-1 compared with the placebo.	Doxorubicin	0-11	programmed cell death 1	Mus musculus	78-82
34094037-10	2021	PD-1 expression was significantly (P<0.05) lower in the group treated with paclitaxel and carboplatin combination as compared with the placebo.	Paclitaxel	75-85	programmed cell death 1	Mus musculus	0-4
34094037-10	2021	PD-1 expression was significantly (P<0.05) lower in the group treated with paclitaxel and carboplatin combination as compared with the placebo.	Carboplatin	90-101	programmed cell death 1	Mus musculus	0-4
34094037-12	2021	Conclusion: Our findings hypothesize that NAC with doxorubicin may potentiate antitumor immunity not merely by recruitment of TILs, but via down-regulation of PD-1 and TIM-3 checkpoints.	nac	42-45	programmed cell death 1	Mus musculus	159-163
34094037-12	2021	Conclusion: Our findings hypothesize that NAC with doxorubicin may potentiate antitumor immunity not merely by recruitment of TILs, but via down-regulation of PD-1 and TIM-3 checkpoints.	Doxorubicin	51-62	programmed cell death 1	Mus musculus	159-163
34094037-13	2021	Carboplatin-containing NAC may suppress PD-1 as well.	Carboplatin	0-11	programmed cell death 1	Mus musculus	40-44
34094037-13	2021	Carboplatin-containing NAC may suppress PD-1 as well.	nac	23-26	programmed cell death 1	Mus musculus	40-44
34117115-0	2021	Mesoporous silica nanoparticles inflame tumors to overcome anti-PD-1 resistance through TLR4-NFkappaB axis.	mesoporous silica	0-17	programmed cell death 1	Mus musculus	64-68
35190830-4	2022	In this study, we found significant diurnal oscillation in the number of PD-1-expressing TAMs collected from B16/BL6 melanoma-bearing mice.	tams	89-93	programmed cell death 1	Mus musculus	73-77
35190830-5	2022	The levels of Pdcd1 mRNA, encoding PD-1, in TAMs also fluctuated in a diurnal manner.	tams	44-48	programmed cell death 1	Mus musculus	14-19
35190830-5	2022	The levels of Pdcd1 mRNA, encoding PD-1, in TAMs also fluctuated in a diurnal manner.	tams	44-48	programmed cell death 1	Mus musculus	35-39
35190830-8	2022	Furthermore, the anti-tumor efficacy of BMS-1, a small molecule inhibitor of PD-1/PD-L1, was enhanced by administering it at the time of day when PD-1 expression increased on TAMs.	tams	175-179	programmed cell death 1	Mus musculus	146-150
35190830-9	2022	These findings suggest that identification of the diurnal expression of PD-1 on TAMs is useful for selecting the most appropriate time of day to administer PD-1/PD-L1 inhibitors.	tams	80-84	programmed cell death 1	Mus musculus	72-76
35190830-9	2022	These findings suggest that identification of the diurnal expression of PD-1 on TAMs is useful for selecting the most appropriate time of day to administer PD-1/PD-L1 inhibitors.	tams	80-84	programmed cell death 1	Mus musculus	156-160
35313341-8	2022	In a third HGSOC model, that had lower inherent IL-6 JAK/STAT3 signaling in the TME but high PD1 signaling, long-term cediranib treatment significantly increased overall survival.	cediranib	118-127	programmed cell death 1	Mus musculus	93-96
35313341-10	2022	Combining cediranib with an anti-PD1 antibody was superior to monotherapy in this model, increasing T cells and decreasing blood vessel densities.	cediranib	10-19	programmed cell death 1	Mus musculus	33-36
35378414-0	2022	Two hydroxyflavanones isolated from Scutellaria baicalensis roots prevent colitis-associated colon cancer in C57BL/6 J mice by inhibiting programmed cell death-1, interleukin 10, and thymocyte selection-associated high mobility group box proteins TOX/TOX2.	hydroxyflavanones	4-21	programmed cell death 1	Mus musculus	138-161
34067957-5	2021	Creatine has been identified as an important metabolic regulator conserving bioenergy to power CD8 T cell antitumor reactivity in a tumor microenvironment; creatine supplementation has been shown to enhance antitumor T cell immunity in multiple preclinical mouse tumor models and, importantly, to synergize with other cancer immunotherapy modalities, such as the PD-1/PD-L1 blockade therapy, to improve antitumor efficacy.	Creatine	0-8	programmed cell death 1	Mus musculus	363-367
35378414-10	2022	CONCLUSION: The inhibitory effects of tetra- and pentahydroxyflavanones on the growth of colon tumors in AOM/DSS-treated mice appear to be associated with decreases in the colon levels of IL-10 and PD-1 through the down-regulated expression of COX-2 and CD8+ T-cell exhaustion by TOX/TOX2 in the tumor microenvironment.	Azoxymethane	105-108	programmed cell death 1	Mus musculus	198-202
35378414-10	2022	CONCLUSION: The inhibitory effects of tetra- and pentahydroxyflavanones on the growth of colon tumors in AOM/DSS-treated mice appear to be associated with decreases in the colon levels of IL-10 and PD-1 through the down-regulated expression of COX-2 and CD8+ T-cell exhaustion by TOX/TOX2 in the tumor microenvironment.	Dextran Sulfate	109-112	programmed cell death 1	Mus musculus	198-202
35395566-11	2022	Moreover, BPYCP administration significantly decreased the percentage of Tfh cells and the expression of Tfh markers ICOS, PD-1 and Bcl-6 in the mesenteric lymph nodes of colitis mice.	bpycp	10-15	programmed cell death 1	Mus musculus	123-127
35378414-9	2022	The administration of 10 mg/kg tetra- and pentahydroxyflavanones to AOM/DSS-treated mice also resulted in decreases of 59.5 and 42.5% in IL-10 levels and 58.1 and 93.9% in PD-1 levels, respectively, in the colon.	tetra- and pentahydroxyflavanones	31-64	programmed cell death 1	Mus musculus	172-176
35378414-9	2022	The administration of 10 mg/kg tetra- and pentahydroxyflavanones to AOM/DSS-treated mice also resulted in decreases of 59.5 and 42.5% in IL-10 levels and 58.1 and 93.9% in PD-1 levels, respectively, in the colon.	Azoxymethane	68-71	programmed cell death 1	Mus musculus	172-176
35378414-9	2022	The administration of 10 mg/kg tetra- and pentahydroxyflavanones to AOM/DSS-treated mice also resulted in decreases of 59.5 and 42.5% in IL-10 levels and 58.1 and 93.9% in PD-1 levels, respectively, in the colon.	Dextran Sulfate	72-75	programmed cell death 1	Mus musculus	172-176
35378414-10	2022	CONCLUSION: The inhibitory effects of tetra- and pentahydroxyflavanones on the growth of colon tumors in AOM/DSS-treated mice appear to be associated with decreases in the colon levels of IL-10 and PD-1 through the down-regulated expression of COX-2 and CD8+ T-cell exhaustion by TOX/TOX2 in the tumor microenvironment.	tetra- and pentahydroxyflavanones	38-71	programmed cell death 1	Mus musculus	198-202
35459193-0	2022	RORgammat agonist enhances anti-PD-1 therapy by promoting monocyte-derived dendritic cells through CXCL10 in cancers.	rorgammat	0-9	programmed cell death 1	Mus musculus	32-36
35525959-9	2022	Moreover, we found that the upregulation of circHMGB2 expression decreased the efficacy of anti-PD-1 therapy, and we revealed that the combination of the CARM1 inhibitor EZM2302 and an anti-PD-1 antibody exerted promising synergistic effects in a preclinical model.	EZM 2302	170-177	programmed cell death 1	Mus musculus	96-100
35367730-0	2022	Reduction of tumor hypoxia by anti-PD-1 therapy assessed using pimonidazole and (18F)FMISO.	fluoromisonidazole	85-90	programmed cell death 1	Mus musculus	35-39
35176418-7	2022	In tumor-bearing mice, the CXCR2 antagonist SB225002 decreased PMN-MDSCs accumulation, increased CD8+ T cells infiltration in GC and further enhanced anti-tumor efficacy of anti-PD-1.	SB 225002	44-52	programmed cell death 1	Mus musculus	178-182
35459193-8	2022	RESULTS: We designed a potent and selective small-molecule RORgammat agonist (8-074) that shows robust antitumor efficacy in syngeneic tumor models and improves the efficacy of anti-PD-1 in a murine lung cancer model.	rorgammat	59-68	programmed cell death 1	Mus musculus	182-186
35459193-12	2022	CONCLUSION: Our results revealed that the RORgammat agonist improved the efficacy of anti-PD-1.	rorgammat	42-51	programmed cell death 1	Mus musculus	90-94
35514996-4	2022	A combination of oral AHCC  and dual immune checkpoint blockade (DICB), including PD-1/CTLA-4 blockade, had reduced tumor growth and increased granzyme B and Ki-67 expression by tumor-infiltrating CD8+ T cells in MC38 colon cancer bearing mice compared to a combination of water and DICB.	Water	273-278	programmed cell death 1	Mus musculus	82-86
35514996-4	2022	A combination of oral AHCC  and dual immune checkpoint blockade (DICB), including PD-1/CTLA-4 blockade, had reduced tumor growth and increased granzyme B and Ki-67 expression by tumor-infiltrating CD8+ T cells in MC38 colon cancer bearing mice compared to a combination of water and DICB.	dicb	283-287	programmed cell death 1	Mus musculus	82-86
35444416-4	2022	Methods: PD-1 antibody and TEPP-46 were integrated by polyethylene glycol (PEG) modified poly (lactic-co-glycolic acid) (PLGA) as a nanoplatform (TPP).	Polyethylene Glycols	54-73	programmed cell death 1	Mus musculus	9-13
35218182-6	2022	ethanol extract (PD1) on 1-chloro-2,4-dinitrochlorobenzene (DNCB)-induced AD-like lesions.	Ethanol	0-7	programmed cell death 1	Mus musculus	17-20
35218182-6	2022	ethanol extract (PD1) on 1-chloro-2,4-dinitrochlorobenzene (DNCB)-induced AD-like lesions.	1,3-Dichloro-2,4-dinitrobenzene	25-58	programmed cell death 1	Mus musculus	17-20
35218182-6	2022	ethanol extract (PD1) on 1-chloro-2,4-dinitrochlorobenzene (DNCB)-induced AD-like lesions.	Dinitrochlorobenzene	60-64	programmed cell death 1	Mus musculus	17-20
35218182-11	2022	Our study demonstrated that PD1 has anti-inflammatory effects, alleviates AD symptoms, inhibits inflammatory responses in skin tissues, and restores barrier function in DNCB-induced AD mice.	Dinitrochlorobenzene	169-173	programmed cell death 1	Mus musculus	28-31
35444416-4	2022	Methods: PD-1 antibody and TEPP-46 were integrated by polyethylene glycol (PEG) modified poly (lactic-co-glycolic acid) (PLGA) as a nanoplatform (TPP).	Polyethylene Glycols	75-78	programmed cell death 1	Mus musculus	9-13
35444416-4	2022	Methods: PD-1 antibody and TEPP-46 were integrated by polyethylene glycol (PEG) modified poly (lactic-co-glycolic acid) (PLGA) as a nanoplatform (TPP).	Polylactic Acid-Polyglycolic Acid Copolymer	89-119	programmed cell death 1	Mus musculus	9-13
35444416-4	2022	Methods: PD-1 antibody and TEPP-46 were integrated by polyethylene glycol (PEG) modified poly (lactic-co-glycolic acid) (PLGA) as a nanoplatform (TPP).	tetraphenylporphine sulfonate	146-149	programmed cell death 1	Mus musculus	9-13
35121624-6	2022	RESULTS: PRS-344/S095012 bound to its targets with high affinity and efficiently blocked the PD-1/PD-L1 pathway, and PRS-344/S095012-mediated 4-1BB co-stimulation was strictly PD-L1 dependent.	s095012	17-24	programmed cell death 1	Mus musculus	93-97
35583057-6	2022	The expression of PD-1after lymphocyte uptake of M-SNP was detected by qPCR.	m-snp	49-54	programmed cell death 1	Mus musculus	18-22
35583057-11	2022	Real-time quantitative PCR results showed that PD-1 expression was significantly down-regulated after M-SNPs uptake by lymphocytes.	m-snps	102-108	programmed cell death 1	Mus musculus	47-51
35355680-0	2022	Carbon ion radiotherapy triggers immunogenic cell death and sensitizes melanoma to anti-PD-1 therapy in mice.	Carbon	0-6	programmed cell death 1	Mus musculus	88-92
35355680-8	2022	Compared with conventional radioimmunotherapy, the combination of CIRT with anti-PD-1 more efficiently triggered traits of immunogenic cell death including the exposure of calreticulin, the release of adenosine triphosphate (ATP), the exodus of high-mobility group box 1 (HMGB1) as well as the induction of type-1 interferon responses.	Adenosine	201-210	programmed cell death 1	Mus musculus	81-85
35355680-8	2022	Compared with conventional radioimmunotherapy, the combination of CIRT with anti-PD-1 more efficiently triggered traits of immunogenic cell death including the exposure of calreticulin, the release of adenosine triphosphate (ATP), the exodus of high-mobility group box 1 (HMGB1) as well as the induction of type-1 interferon responses.	Adenosine Triphosphate	225-228	programmed cell death 1	Mus musculus	81-85
35217343-0	2022	Enhancement of anti-PD-1/PD-L1 immunotherapy for osteosarcoma using an intelligent autophagy-controlling metal organic framework.	Metals	105-110	programmed cell death 1	Mus musculus	20-24
35347072-13	2022	Furthermore, eEF2K inhibitor, NH125 treatment or eEF2K knockdown enhanced the efficacy of PD-1 mAb therapy in a melanoma mouse model.	NH 125	30-35	programmed cell death 1	Mus musculus	90-94
35251033-8	2022	Although no signs of hyperinflammatory toxicity were observed, mice with IPM receiving ICIs, particularly anti-PD-1, had elevated serum levels of IL-6, a cytokine linked to ICI toxicities.	ipm	73-76	programmed cell death 1	Mus musculus	111-115
35251033-9	2022	Altogether, inhibition of the PD-1/PD-L1 pathway improved clinical outcomes of IPM in immunosuppressed mice, even without concomitant antifungals.	ipm	79-82	programmed cell death 1	Mus musculus	30-34
35178106-12	2022	Results: The mRNA and protein expression levels of AFP, PD-1, CTLA-4, and IL-10 were significantly downregulated in the CIAA-treated mice in comparison with HCC mice.	ciaa	120-124	programmed cell death 1	Mus musculus	56-60
35222421-8	2022	In NSG mice bearing RPMI-8226 tumors overexpressing TGF-beta, the B2ARM CAR mediated 100% tumor rejection and survival, superior infiltration of tumors on day 7 post CAR T treatment (%CD3+CAR+), and greater expression of IFN-gamma, TNF-alpha, Ki67, Granzyme B, and PD-1, as compared to tumor-infiltrating non-armored B2 CAR T-cells.	rpmi-8226	20-29	programmed cell death 1	Mus musculus	265-269
35115804-6	2022	Inflammatory infiltrate scores, alveoli deformation scores, collagen volume fractions and hydroxyproline contents in lung tissues were all significantly higher in mice administered PD-1 inhibitor plus irradiation than in the other three groups.	Hydroxyproline	90-104	programmed cell death 1	Mus musculus	181-185
35145222-6	2022	This GABA-mediated beta-catenin activation both stimulates tumour cell proliferation and suppresses CD8+ T cell intratumoural infiltration, such that targeting GAD1 or GABABR in mouse models overcomes resistance to anti-PD-1 immune checkpoint blockade therapy.	gamma-Aminobutyric Acid	5-9	programmed cell death 1	Mus musculus	220-224
35096487-8	2022	C3 subtype GBMs were enriched with TC-6 cells and immunosuppressive TAMs, and exhibited an immunomodulatory signature that associated with reduced efficacy of anti-PD-1 treatment.	Technetium	35-37	programmed cell death 1	Mus musculus	164-168
35127555-9	2021	Higher level of CD69, ICOS and PD-1, lower level of CD62L, and decreased IFN-gamma producing after stimulation by PMA and ionomycin were found in gammadeltaT cells from infected mice, compared with naive mice.	Tetradecanoylphorbol Acetate	114-117	programmed cell death 1	Mus musculus	31-35
35075146-7	2022	Experiments with mouse xenograft models of pancreatic cancer showed that TH-Z835 significantly reduced tumor volume and synergized with an anti-PD-1 antibody.	th-z835	73-80	programmed cell death 1	Mus musculus	144-148
35086457-15	2022	Furthermore, UC-MSC-derived PGE2 enhanced PD-L1 expression in RAW264.7 cells, which in turn promoted programmed cell death protein 1 (PD-1) expression and reduced IL-2 and IFN-gamma production in Jurkat T cells.	Dinoprostone	28-32	programmed cell death 1	Mus musculus	101-132
35086457-15	2022	Furthermore, UC-MSC-derived PGE2 enhanced PD-L1 expression in RAW264.7 cells, which in turn promoted programmed cell death protein 1 (PD-1) expression and reduced IL-2 and IFN-gamma production in Jurkat T cells.	Dinoprostone	28-32	programmed cell death 1	Mus musculus	134-138
33945995-10	2021	The results indicated that oncolytic VACV with Western Reserve-mediated anti-human-PD-1 and anti-human-4-1BB antibody co-expression exerted a significant antitumor effect, indicating that the combination of oncolytic virotherapy and immunotherapy by the oncolytic VACV expressing one or more immune checkpoint genes might have satisfactory clinical expectations.	Valacyclovir	37-41	programmed cell death 1	Mus musculus	83-87
35058524-7	2022	Tumor size was significantly reduced in mice treated with CC-01 combined with or without anti-PD-1 antibody, however the triple combination therapy consistently demonstrated that it significantly increased both the ORR and survival rate in term of clinical applications.	cc-01	58-63	programmed cell death 1	Mus musculus	94-98
35115949-12	2021	This study suggested that combination of the FAK inhibitor VS4718 and anti-PD1 could be a potential therapy for HCC by improving the immune environment, reducing liver fibrosis and simultaneously preventing PD1 from binding to the increased PD-L1 induced by FAK inhibitor VS4718.	PND 1186	59-65	programmed cell death 1	Mus musculus	207-210
35115949-12	2021	This study suggested that combination of the FAK inhibitor VS4718 and anti-PD1 could be a potential therapy for HCC by improving the immune environment, reducing liver fibrosis and simultaneously preventing PD1 from binding to the increased PD-L1 induced by FAK inhibitor VS4718.	PND 1186	272-278	programmed cell death 1	Mus musculus	75-78
35115949-12	2021	This study suggested that combination of the FAK inhibitor VS4718 and anti-PD1 could be a potential therapy for HCC by improving the immune environment, reducing liver fibrosis and simultaneously preventing PD1 from binding to the increased PD-L1 induced by FAK inhibitor VS4718.	PND 1186	272-278	programmed cell death 1	Mus musculus	207-210
35015785-7	2022	In mice experiments with ADT and various combinations of PD-1 and CTLA-4 inhibitors, tumor volume at day 30 was always larger than the initial tumor.	adt	25-28	programmed cell death 1	Mus musculus	57-61
35015785-9	2022	Although the treatment with ADT in combination with PD-1 inhibitor or CTLA-4 inhibitor has been disappointing in clinical trials, our simulations suggest that, disregarding negative effects, combinations of ADT with checkpoint inhibitors can be effective in reducing tumor volume if larger doses are used.	adt	28-31	programmed cell death 1	Mus musculus	52-56
35015785-9	2022	Although the treatment with ADT in combination with PD-1 inhibitor or CTLA-4 inhibitor has been disappointing in clinical trials, our simulations suggest that, disregarding negative effects, combinations of ADT with checkpoint inhibitors can be effective in reducing tumor volume if larger doses are used.	adt	207-210	programmed cell death 1	Mus musculus	52-56
34980222-0	2022	Prevotellaceae produces butyrate to alleviate PD-1/PD-L1 inhibitor-related cardiotoxicity via PPARalpha-CYP4X1 axis in colonic macrophages.	Butyrates	24-32	programmed cell death 1	Mus musculus	46-50
34980222-3	2022	METHODS: A mouse model of immune checkpoint inhibitor-related cardiotoxicity was constructed by PD-1/PD-L1 inhibitor BMS-1 (5 and 10 mg/kg), and cardiomyocyte apoptosis and cardiotoxicity were determined by hematoxylin and eosin, Masson"s trichome and TUNEL assays.	Hematoxylin	207-218	programmed cell death 1	Mus musculus	96-100
34980222-3	2022	METHODS: A mouse model of immune checkpoint inhibitor-related cardiotoxicity was constructed by PD-1/PD-L1 inhibitor BMS-1 (5 and 10 mg/kg), and cardiomyocyte apoptosis and cardiotoxicity were determined by hematoxylin and eosin, Masson"s trichome and TUNEL assays.	Eosine Yellowish-(YS)	223-228	programmed cell death 1	Mus musculus	96-100
34980222-13	2022	Importantly, Prevotella loescheii recolonization and butyrate supplementation alleviated PD-1/PD-L1 inhibitor-related cardiotoxicity.	Butyrates	53-61	programmed cell death 1	Mus musculus	89-93
34980222-15	2022	CONCLUSIONS: Intestinal barrier dysfunction amplifies PD-1/PD-L1 inhibitor-related cardiotoxicity by upregulating proinflammatory factors TNF-alpha and IL-1beta in colonic macrophages via downregulation of butyrate-PPARalpha-CYP4X1 axis.	Butyrates	206-214	programmed cell death 1	Mus musculus	54-58
35003748-0	2022	SKI-G-801, an AXL kinase inhibitor, blocks metastasis through inducing anti-tumor immune responses and potentiates anti-PD-1 therapy in mouse cancer models.	ski-g-801	0-9	programmed cell death 1	Mus musculus	120-124
34007176-7	2021	The immunotherapeutic mechanism initially demonstrated that when tumor cells were transfected by sPD-1 delivered by NBs, which downregulated the expression of programmed death-ligand 1 (PD-L1) in tumor cells, and blocked the PD-1/PD-L1 signaling pathway, which improved T-cell-mediated tumor inhibition.	Bromosuccinimide	116-119	programmed cell death 1	Mus musculus	98-102
34052328-6	2021	Both luteolin and apigenin showed potent anti-cancer activities in the H358 xenograft and Lewis lung carcinoma model in vivo, and the treatment with monoclonal PD1 antibody enhanced the infiltration of T cells into tumor tissues.	Luteolin	5-13	programmed cell death 1	Mus musculus	160-163
34036623-4	2021	Consistently, in C57BL/6 wild-type mice receiving anti-PD-1 therapy, PD-L1 expression and Treg infiltration in subcutaneous tumors reduced when adding lenvatinib to the scheme.	lenvatinib	151-161	programmed cell death 1	Mus musculus	55-59
33744709-7	2021	Besides, in a murine SCI model using T-and-B-cell-deficient Rag1-/- mice, Treg-specific PD-1 knockdown impairs Treg-mediated neuroprotection in vivo, as evidenced by enlarged lesion area.	treg	74-78	programmed cell death 1	Mus musculus	88-92
33744709-8	2021	Taken together, our study revealed that PD-1, which is upregulated on infiltrating Tregs in the subacute phase of SCI, is essential for Tregs to maintain Foxp3 expression and anti-inflammatory activity to counteract the effect of pro-inflammatory macrophages and microglia.	tregs	83-88	programmed cell death 1	Mus musculus	40-44
33744709-8	2021	Taken together, our study revealed that PD-1, which is upregulated on infiltrating Tregs in the subacute phase of SCI, is essential for Tregs to maintain Foxp3 expression and anti-inflammatory activity to counteract the effect of pro-inflammatory macrophages and microglia.	tregs	136-141	programmed cell death 1	Mus musculus	40-44
34037385-0	2021	Design, Synthesis, and Evaluation of o-(Biphenyl-3-ylmethoxy)nitrophenyl Derivatives as PD-1/PD-L1 Inhibitors with Potent Anticancer Efficacy In Vivo.	-(biphenyl-3-ylmethoxy)nitrophenyl derivatives	38-84	programmed cell death 1	Mus musculus	88-92
34037385-1	2021	Two series of novel o-(biphenyl-3-ylmethoxy)nitrophenyl compounds (A1-31 and B1-17) were designed as programmed cell death protein 1 (PD-1)/PD-ligand 1 (PD-L1) inhibitors.	o-(biphenyl-3-ylmethoxy)nitrophenyl	20-55	programmed cell death 1	Mus musculus	101-132
34037385-1	2021	Two series of novel o-(biphenyl-3-ylmethoxy)nitrophenyl compounds (A1-31 and B1-17) were designed as programmed cell death protein 1 (PD-1)/PD-ligand 1 (PD-L1) inhibitors.	o-(biphenyl-3-ylmethoxy)nitrophenyl	20-55	programmed cell death 1	Mus musculus	134-138
34031449-8	2021	nor-NOHA administration increased dendritic and T cell tumor-infiltration and PD-1 expression.	norLeu3-A(1-7)	0-8	programmed cell death 1	Mus musculus	78-82
34031449-9	2021	The combination of nor-NOHA and anti-PD-1 therapy with nivolumab enhanced anti-PD-1 therapeutic efficacy.	norLeu3-A(1-7)	19-27	programmed cell death 1	Mus musculus	79-83
33744709-4	2021	In the current research, we applied a murine SCI model to demonstrate the upregulation of programmed death protein 1(PD-1) in infiltrating Tregs and significant expression of programmed death-ligand 1 (PD-L1) on post-SCI macrophages/microglia.	tregs	139-144	programmed cell death 1	Mus musculus	117-121
33744709-5	2021	Furthermore, through using an inducible shRNA lentivirus system, we showed that Treg-specific PD-1 knockdown impairs the anti-inflammatory function of infiltrating Tregs.	tregs	164-169	programmed cell death 1	Mus musculus	94-98
33744709-6	2021	PD-1 is crucial for the maintenance of Treg identity and function under the influence of pro-inflammatory macrophages/microglia, and PD-1-deficient Tregs are less competent to inhibit pro-inflammatory macrophages/microglia.	treg	39-43	programmed cell death 1	Mus musculus	0-4
33593880-7	2021	RESULTS: Single cell RNA sequencing of murine tumors identified a CXCR3 gene signature (CXCR3-GS) following Tavo treatment associated with enhanced antigen presentation, T cell infiltration and expansion, and PD-1/PD-L1 expression.	tavo	108-112	programmed cell death 1	Mus musculus	209-213
33980416-7	2021	RESULTS: Treatment with melphalan-based therapy significantly induced the expression of PD-1 on CD8+ tumour-infiltrating lymphocytes.	Melphalan	24-33	programmed cell death 1	Mus musculus	88-92
33980416-9	2021	CONCLUSIONS: This study thus suggests that the addition of PD-1 blockade to melphalan-based therapies, such as ILP, may be therapeutically beneficial.	Melphalan	76-85	programmed cell death 1	Mus musculus	59-63
33656040-8	2021	This is the first study to show that CDDP-NPs can amplify RT-induced immune activation and break through the efficiency limitation of the RT plus anti-PD1 induced abscopal effect.	Cisplatin	37-41	programmed cell death 1	Mus musculus	151-154
34016722-8	2021	Importantly, in vivo clotrimazole administration induced intratumor immune infiltration and inhibited tumor growth depending on both DCs and CD8+ T cells and potentiated the antitumor efficacy of anti-PD1 antibody.	Clotrimazole	21-33	programmed cell death 1	Mus musculus	201-204
34016722-9	2021	CONCLUSIONS: Our findings showed that clotrimazole could trigger DC activation via the lactate-lysosome axis to promote antigen cross-presentation and could be used as a potential combination therapy approach to improving the therapeutic efficacy of anti-PD1 immunotherapy.	Clotrimazole	38-50	programmed cell death 1	Mus musculus	255-258
33656040-0	2021	Cisplatin nanoparticles boost abscopal effect of radiation plus anti-PD1 therapy.	Cisplatin	0-9	programmed cell death 1	Mus musculus	69-72
33129954-5	2021	In the mouse model, imatinib suppressed stromal reaction and increased sensitivity to anti-PD-1 treatment in excluded-type CRC.	Imatinib Mesylate	20-28	programmed cell death 1	Mus musculus	91-95
33428059-8	2021	AMD3100, an antagonist for CXCR4 receptor inhibited PD-1 expression in BMDCs suggesting that PD-1 induction requires CXCL12.	plerixafor	0-7	programmed cell death 1	Mus musculus	52-56
33428059-8	2021	AMD3100, an antagonist for CXCR4 receptor inhibited PD-1 expression in BMDCs suggesting that PD-1 induction requires CXCL12.	plerixafor	0-7	programmed cell death 1	Mus musculus	93-97
33758937-8	2021	We then treated mice with T3 to confirm the effect of thyroid hormone on PD-1 expression in Tregs and Tregs function in vivo.	tregs	92-97	programmed cell death 1	Mus musculus	73-77
33758937-11	2021	High levels of circulating T3 reduced PD-1 expression in Tregs, impaired Tregs function, and disrupted T-helper cell (Th1 and Th2) balance in mice treated with T3.	Triiodothyronine	27-29	programmed cell death 1	Mus musculus	38-42
33796403-4	2021	EP4 inhibition by MF-766 synergistically improved the efficacy of anti-programmed cell death protein 1 (PD-1) therapy in CT26 and EMT6 syngeneic tumor mouse models.	MF-766	18-24	programmed cell death 1	Mus musculus	71-102
33796403-4	2021	EP4 inhibition by MF-766 synergistically improved the efficacy of anti-programmed cell death protein 1 (PD-1) therapy in CT26 and EMT6 syngeneic tumor mouse models.	MF-766	18-24	programmed cell death 1	Mus musculus	104-108
33529880-5	2021	We demonstrated that a small molecule compound (N-[2-(aminocarbonyl)phenyl][1,1"-biphenyl]-4-carboxamide [APBC]) could effectively interrupt the PD-1/PD-L1 interaction by directly binding to PD-L1, presenting the KD and IC50 values at low-micromolar level.	n-[2-(aminocarbonyl)phenyl][1,1"-biphenyl]-4-carboxamide	48-104	programmed cell death 1	Mus musculus	145-149
33529880-5	2021	We demonstrated that a small molecule compound (N-[2-(aminocarbonyl)phenyl][1,1"-biphenyl]-4-carboxamide [APBC]) could effectively interrupt the PD-1/PD-L1 interaction by directly binding to PD-L1, presenting the KD and IC50 values at low-micromolar level.	apbc	106-110	programmed cell death 1	Mus musculus	145-149
33529880-6	2021	Molecular docking study revealed that APBC may have function through a PD-L1 dimer-locking mechanism, occluding the PD-1 interaction surface of PD-L1.	apbc	38-42	programmed cell death 1	Mus musculus	116-120
33511398-7	2021	In recipient lymphoid tissues, lack of donor T cell PD-1 interaction with tissue-PD-L1 preserved donor PD-1+TCF-1+Ly108+CD8+ T memory progenitors (Tmp) and functional effectors that have strong GVL activity.	ly108	114-119	programmed cell death 1	Mus musculus	52-56
33870463-13	2021	CONCLUSIONS: By successful uncoupling of the PD-1/PD-L1 axis, we provide further evidence for the safe and successful application of immunotherapies to combat dMMR-driven malignancies that warrants further investigation.	dmmr	159-163	programmed cell death 1	Mus musculus	45-49
33896829-6	2021	Tongue tissues from mice treated with 4NQO for 12 weeks had higher levels of Th2 cells and Tregs compared to tissues taken from control mice or mice treated with 4NQO for 28 weeks; these results suggested a potential therapeutic benefit of anti-PD-1 in the oral cancer.	4-Nitroquinoline-1-oxide	38-42	programmed cell death 1	Mus musculus	245-249
33896829-6	2021	Tongue tissues from mice treated with 4NQO for 12 weeks had higher levels of Th2 cells and Tregs compared to tissues taken from control mice or mice treated with 4NQO for 28 weeks; these results suggested a potential therapeutic benefit of anti-PD-1 in the oral cancer.	4-Nitroquinoline-1-oxide	162-166	programmed cell death 1	Mus musculus	245-249
33896829-8	2021	Inhibition of IL-17alpha combined with PD-1 blockade delayed the development of 4NQO-induced precancerous and cancerous lesions and prolonged the survival of 4NQO-treated mice.	4-Nitroquinoline-1-oxide	80-84	programmed cell death 1	Mus musculus	39-43
33896829-8	2021	Inhibition of IL-17alpha combined with PD-1 blockade delayed the development of 4NQO-induced precancerous and cancerous lesions and prolonged the survival of 4NQO-treated mice.	4-Nitroquinoline-1-oxide	158-162	programmed cell death 1	Mus musculus	39-43
33677010-1	2021	This study investigates the effect of PD1 blockade on the therapeutic efficacy of novel doxorubicin-loaded temperature-sensitive liposomes.	Doxorubicin	88-99	programmed cell death 1	Mus musculus	38-41
33509790-9	2021	Targeting the Janus Kinase (JAK)/STAT signaling pathway using the FDA approved drug ruxolitinib overcame these tumor-protective responses and improved anti-PD-1 therapeutic efficacy.	ruxolitinib	84-95	programmed cell death 1	Mus musculus	156-160
33859941-0	2021	Inhibition of LDH-A by Oxamate Enhances the Efficacy of Anti-PD-1 Treatment in an NSCLC Humanized Mouse Model.	Oxamic Acid	23-30	programmed cell death 1	Mus musculus	61-65
33757978-5	2021	Preclinical mouse tumor modeling showed that depletion of CCR8+ Tregs through an FcyR engaging anti-CCR8 antibody, but not blockade, enabled dose-dependent, effective, and long-lasting antitumor immunity that synergized with PD-1 blockade.	tregs	64-69	programmed cell death 1	Mus musculus	225-229
33751208-14	2021	In a mouse model, adding anti-PD-1 antibody to the combination of CHP-NY-ESO-1/poly-ICLC suppressed the growth of NY-ESO-1-expressing tumors.	poly	79-83	programmed cell death 1	Mus musculus	30-34
33388950-0	2021	Pingyangmycin enhances the antitumor efficacy of anti-PD-1 therapy associated with tumor-infiltrating CD8+ T cell augmentation.	bleomycetin	0-13	programmed cell death 1	Mus musculus	54-58
33717088-8	2021	Moreover, activated CD8+ T cells treated with bortezomib exhibited a significant reduction in programmed cell death-1 (PD-1) expressing SHIP1+ phenotype.	Bortezomib	46-56	programmed cell death 1	Mus musculus	119-123
33717088-9	2021	These data underscore a mechanism of action by which bortezomib induces miR-155-dependent downregulation of SOCS1 and SHIP1 negative regulatory proteins, leading to a suppressed PD-1-mediated T cell exhaustion.	Bortezomib	53-63	programmed cell death 1	Mus musculus	178-182
33754054-16	2021	In addition, we identified unique bacterial modules that were significantly enriched in the anti-PD-1 mAb + pectin group, which composed of butyrate-producing bacteria indicative of good response to immunotherapy.	Butyrates	140-148	programmed cell death 1	Mus musculus	97-101
33754054-18	2021	Furthermore, butyrate, a main product of dietary fiber in gut microbial fermentation, was found to be sufficient to promote T cells infiltration and thus enhance the efficacy of anti-PD-1 mAb.	Butyrates	13-21	programmed cell death 1	Mus musculus	183-187
33536206-4	2021	Coadministration of the TGF-beta receptor inhibitor galunisertib and chemotherapy drugs provoked vigorous antitumor activity of anti-PD-1 therapy in mouse tumor models.	LY-2157299	52-64	programmed cell death 1	Mus musculus	133-137
32533100-0	2021	Apatinib prevents natural killer cell dysfunction to enhance the efficacy of anti-PD-1 immunotherapy in hepatocellular carcinoma.	apatinib	0-8	programmed cell death 1	Mus musculus	82-86
33129844-9	2021	The combination of 5-fluorouracil and oxaliplatin reduced MDSCs, increased numbers of intra-tumor CD8+ T cells, and increased the response of tumors to anti-PD1-however, this resulted in increased tumor expression of PDL1.	Fluorouracil	19-33	programmed cell death 1	Mus musculus	157-160
33129844-9	2021	The combination of 5-fluorouracil and oxaliplatin reduced MDSCs, increased numbers of intra-tumor CD8+ T cells, and increased the response of tumors to anti-PD1-however, this resulted in increased tumor expression of PDL1.	Oxaliplatin	38-49	programmed cell death 1	Mus musculus	157-160
33129844-12	2021	CONCLUSIONS: In mouse models of gastric cancer, 5-fluorouracil and oxaliplatin reduce numbers of MDSCs to increase the effects of anti-PD1, which promotes tumor infiltration by CD8+ T cells.	Fluorouracil	48-62	programmed cell death 1	Mus musculus	135-138
33129844-12	2021	CONCLUSIONS: In mouse models of gastric cancer, 5-fluorouracil and oxaliplatin reduce numbers of MDSCs to increase the effects of anti-PD1, which promotes tumor infiltration by CD8+ T cells.	Oxaliplatin	67-78	programmed cell death 1	Mus musculus	135-138
33430352-9	2021	Therefore, the combination of cisplatin and irradiation induces immunogenic cell death and potentiates postirradiation anti-PD-1 treatment efficacy in UC.	Cisplatin	30-39	programmed cell death 1	Mus musculus	124-128
33584714-4	2020	Herein, we report stabilization of tumor blood vessels by endothelial dysfunctional blocker CU06-1004, which modified the TME and showed synergistic effects with immunotherapy anti-PD-1 antibody.	cu06-1004	92-101	programmed cell death 1	Mus musculus	181-185
33584714-9	2020	Taken together, our findings suggest that CU06-1004 is a potential candidate drug capable of improving therapeutic efficacy of anti-PD-1 through beneficial changes in the TME.	cu06-1004	42-51	programmed cell death 1	Mus musculus	132-136
33151910-6	2021	Combining PD-1 blockade with Birc2/3 antagonism in mice reduced IPCs and enhanced tumor cell killing in vivo, resulting in durable responsiveness that matched TNF cytotoxicity thresholds in vitro.	ipcs	64-68	programmed cell death 1	Mus musculus	10-14
33300057-0	2021	The mRNA expression of Il6 and Pdcd1 are predictive and protective factors for doxorubicin-induced cardiotoxicity.	Doxorubicin	79-90	programmed cell death 1	Mus musculus	31-36
33320838-0	2021	Ketogenic diet and ketone bodies enhance the anticancer effects of PD1 blockade.	Ketones	19-25	programmed cell death 1	Mus musculus	67-70
33520112-6	2021	Moreover, we found an improved therapeutic effect when YUMM tumor-bearing mice were treated with TA99 combined with MEKi and immune checkpoint blockade (anti-PD1 and anti-CTLA4).	ta99	97-101	programmed cell death 1	Mus musculus	158-161
33430352-0	2021	Combination of Cisplatin and Irradiation Induces Immunogenic Cell Death and Potentiates Postirradiation Anti-PD-1 Treatment Efficacy in Urothelial Carcinoma.	Cisplatin	15-24	programmed cell death 1	Mus musculus	109-113
33495297-13	2021	A metronomic dose of olaparib was highly synergistic with anti-PD-1-based immunotherapy, leading to eradication of MSIhigh or reduction of MSS tumors in mice.	olaparib	21-29	programmed cell death 1	Mus musculus	63-67
32467569-0	2021	CS1003, a novel human and mouse cross-reactive PD-1 monoclonal antibody for cancer therapy.	5-(pyrazin-2-yl)pyridin-2-amine	0-6	programmed cell death 1	Mus musculus	47-51
33462142-13	2021	S-equol facilitates TCR activation that stimulates the ERbeta phosphotyrosine switch and boosts anti-PD-1 (Programmed cell death protein 1) ICB immunotherapy.Our mouse genetic study clearly demonstrates a role of the ERbeta phosphotyrosine switch in regulating ERbeta-dependent antitumor immunity in CD8+ T cells.	Equol	0-7	programmed cell death 1	Mus musculus	101-105
33462142-13	2021	S-equol facilitates TCR activation that stimulates the ERbeta phosphotyrosine switch and boosts anti-PD-1 (Programmed cell death protein 1) ICB immunotherapy.Our mouse genetic study clearly demonstrates a role of the ERbeta phosphotyrosine switch in regulating ERbeta-dependent antitumor immunity in CD8+ T cells.	Equol	0-7	programmed cell death 1	Mus musculus	107-138
33074129-0	2021	Rova-T enhances the anti-tumor activity of anti-PD1 in a murine model of small cell lung cancer with endogenous Dll3 expression.	rovalpituzumab tesirine	0-6	programmed cell death 1	Mus musculus	48-51
33074129-3	2021	Using a pre-clinical murine SCLC tumor model that expresses Dll3 and has an intact murine immune system, we found that sub-efficacious doses of Rova-T with anti-PD1 resulted in enhanced anti-tumor activity, compared to either monotherapy.	rovalpituzumab tesirine	144-150	programmed cell death 1	Mus musculus	161-164
33074129-7	2021	Whole transcriptome analysis as well as flow cytometry and IHC showed that Rova-T activates dendritic cells and increases Ccl5, Il-12, and Icam more than anti-PD1 alone.	rovalpituzumab tesirine	75-81	programmed cell death 1	Mus musculus	159-162
33074129-8	2021	Increased tumor expression of PDL1 and MHC1 following Rova-T treatment also supports combination with anti-PD1.	rovalpituzumab tesirine	54-60	programmed cell death 1	Mus musculus	107-110
33155587-0	2020	Selection of threose nucleic acid aptamers to block PD-1/PD-L1 interaction for cancer immunotherapy.	erythrose	13-20	programmed cell death 1	Mus musculus	52-56
33490922-6	2021	Significantly, intraperitoneal transfer of cisplatin-induced, SASP-boosted senescent cells with irinotecan sensitizes ovarian tumor to anti-PD-1 antibody and improves the survival of tumor-bearing mice in an immunocompetent, syngeneic model.	Cisplatin	43-52	programmed cell death 1	Mus musculus	140-144
33490900-3	2021	Anti-PD1 therapy-sensitive tumor lines MC38, CT26, and RIL-175 were used to investigate the impact of HCQ on anti-PD1 therapy efficacy.	Hydroxychloroquine	102-105	programmed cell death 1	Mus musculus	114-117
33490900-6	2021	Importantly, in all the three tumor models, HCQ treatment significantly impaired the response to anti-PD1 treatment, accompanying diminished in vivo T-cell activation and reduced tumor-infiltrating, antigen-specific CD8+ T cells.	Hydroxychloroquine	44-47	programmed cell death 1	Mus musculus	102-105
33490900-0	2021	Hydroxychloroquine can impair tumor response to anti-PD1 in subcutaneous mouse models.	Hydroxychloroquine	0-18	programmed cell death 1	Mus musculus	53-56
33490900-2	2021	Here, we evaluate the influence of HCQ treatment on the effect of anti-PD1 tumor immunotherapy.	Hydroxychloroquine	35-38	programmed cell death 1	Mus musculus	71-74
33155587-1	2020	Threose nucleic acid (TNA) aptamers were selected in vitro to bind PD-L1 protein and inhibit its interaction with PD-1.	erythrose	0-7	programmed cell death 1	Mus musculus	114-118
33263448-7	2020	Furthermore, we demonstrated that 3D OI/CT can also image the therapeutic distribution of a Cy7-labeled anti-PD-1 antibody, a prototype translational antibody therapy.	cyanine dye 7	92-95	programmed cell death 1	Mus musculus	109-113
33263448-8	2020	We successfully imaged real-time antibody distribution after HIFU-induced BBB permeability, which correlated with post necropsy Cy7 signal and translational PET imaging after injection of [89Zr] anti-PD-1 antibody.	hifu	61-65	programmed cell death 1	Mus musculus	200-204
33511018-3	2021	Here, a FePSe3-based theranostic agent, FePSe3@APP@CCM, loaded with anti-PD-1 peptide (APP) as the inner component and CT26 cancer cell membrane (CCM) as the outer shell is reported, which acts as a multifunctional agent for MR and PA imaging and photothermal and immunotherapy against cancer.	Protactinium	232-234	programmed cell death 1	Mus musculus	73-77
33028620-9	2020	Finally, the enhanced antitumor effect of fruquintinib/anti-PD-1 cotreatment was significantly reversed in CD8 knockout mice compared with that in the wild-type mice.	HMPL-013	42-54	programmed cell death 1	Mus musculus	60-64
33186040-1	2020	A series of novel linear aliphatic amine-linked triaryl derivatives as inhibitors of PD-1/PD-L1 were designed, synthesized, and evaluated in vitro and in vivo.	Amines	35-40	programmed cell death 1	Mus musculus	85-89
33186040-1	2020	A series of novel linear aliphatic amine-linked triaryl derivatives as inhibitors of PD-1/PD-L1 were designed, synthesized, and evaluated in vitro and in vivo.	triaryl	48-55	programmed cell death 1	Mus musculus	85-89
33329575-13	2020	Conclusively, combination treatment with ACY738 augmented the antitumor efficacy of anti-PD-1 and anti-PD-L1 monoclonal antibodies in the Emu-TCL1 adoptive transfer murine model.	N-hydroxy-2-(1-phenylcycloproylamino)pyrimidine-5-carboxamide	41-47	programmed cell death 1	Mus musculus	89-93
33147777-0	2020	Unripe Black Raspberry (Rubus coreanus Miquel) Extract and Its Constitute, Ellagic Acid Induces T Cell Activation and Antitumor Immunity by Blocking PD-1/PD-L1 Interaction.	Ellagic Acid	75-87	programmed cell death 1	Mus musculus	149-153
33148223-13	2020	RX-5902 also was shown to potentiate the effects of checkpoint inhibitors of CTLA4 and the PD-1 inhibitor in the 4 T-1 murine TNBC model.	RX-5902	0-7	programmed cell death 1	Mus musculus	91-95
33171765-11	2020	Conclusively, the combination of FlaB-Vax with PDT-mediated tumor ablation would serve a safe and feasible combinatorial therapy for enhancing PD-1 blockade treatment of malignant melanoma.	flab	33-37	programmed cell death 1	Mus musculus	143-147
32758571-4	2020	The three dihydroxystilbenes inhibited colon carcinogenesis and tumor growth as well as increases in colon IL-1beta, IL-6, MCP-1, and PD-1 levels in AOM/DDS-treated mice (in vivo).	dihydroxystilbenes	10-28	programmed cell death 1	Mus musculus	134-138
32758571-6	2020	The results obtained also revealed that the three dihydroxystilbenes inhibited PD-1 elevations in M2-THP-1 macrophages (in vitro).	dihydroxystilbenes	50-68	programmed cell death 1	Mus musculus	79-83
32758571-7	2020	Therefore, the inhibition of AOM/DSS-induced colon carcinogenesis and colon tumor growth by 2,3-, 3,4-, and 4,4"-dihydroxystilbenes appears to be due to the suppression of M2 TAM differentiation and activation and PD-1 expression (immunosuppression) via reductions in COX-2 expression levels in the colon tumor microenvironment.	Azoxymethane	29-32	programmed cell death 1	Mus musculus	214-218
32758571-7	2020	Therefore, the inhibition of AOM/DSS-induced colon carcinogenesis and colon tumor growth by 2,3-, 3,4-, and 4,4"-dihydroxystilbenes appears to be due to the suppression of M2 TAM differentiation and activation and PD-1 expression (immunosuppression) via reductions in COX-2 expression levels in the colon tumor microenvironment.	Dextran Sulfate	33-36	programmed cell death 1	Mus musculus	214-218
32758571-7	2020	Therefore, the inhibition of AOM/DSS-induced colon carcinogenesis and colon tumor growth by 2,3-, 3,4-, and 4,4"-dihydroxystilbenes appears to be due to the suppression of M2 TAM differentiation and activation and PD-1 expression (immunosuppression) via reductions in COX-2 expression levels in the colon tumor microenvironment.	2,3-, 3,4-, and 4,4"-dihydroxystilbenes	92-131	programmed cell death 1	Mus musculus	214-218
33147777-9	2020	RCE and ellagic acid dose-dependently block the binding of PD-1 to PD-L1.	Ellagic Acid	8-20	programmed cell death 1	Mus musculus	59-63
32948683-7	2020	PD-1 and CTLA-4 were upregulated on tumor-infiltrating CD4+ and CD8+ T cells in irradiated and nonirradiated tumors, suggesting that immune checkpoint inhibitors could be beneficial after LRT and Foxp3+ Treg depletion.	treg	203-207	programmed cell death 1	Mus musculus	0-4
32839553-11	2020	Combining Mn2+ with immune checkpoint inhibition synergistically boosted antitumor efficacies and reduced the anti-PD-1 antibody dosage required in mice.	Manganese(2+)	10-14	programmed cell death 1	Mus musculus	115-119
33243934-3	2020	To improve the efficacy, the immune-chemotherapy combination with pemetrexed, cis/carboplatin and pembrolizumab (anti-PD-1) has been recently approved as first-line treatment in advanced NSCLCs.	Pemetrexed	66-76	programmed cell death 1	Mus musculus	118-122
33243934-9	2020	RESULTS: Pemetrexed induced the transcriptional activation of PD-L1 (encoded by CD274) by inactivating thymidylate synthase (TS) in NSCLC cells and, in turn, activating T-lymphocytes when combined with the anti-PD-1/PD-L1 therapy.	Pemetrexed	9-19	programmed cell death 1	Mus musculus	211-215
33188035-10	2020	CONCLUSION: The combination of anti-PD-1 antibody immunotherapy with GEM was beneficial to treat a murine model of PDAC liver metastasis by enhancing the immune response mediated by Th1 lymphocytes and M1 macrophages and was associated with CD8+ T cells.	gemcitabine	69-72	programmed cell death 1	Mus musculus	36-40
33176206-0	2020	Discrepant antitumor efficacies of three CpG oligodeoxynucleotide classes in monotherapy and co-therapy with PD-1 blockade.	Oligodeoxyribonucleotides	45-65	programmed cell death 1	Mus musculus	109-113
33176206-5	2020	CpG-B at low doses significantly inhibited tumor growth and possessed synergistic antitumor effects with the anti-PD-1 antibody.	cpg-b	0-5	programmed cell death 1	Mus musculus	114-118
33117347-0	2020	Excretory/Secretory Products From Trichinella spiralis Adult Worms Attenuated DSS-Induced Colitis in Mice by Driving PD-1-Mediated M2 Macrophage Polarization.	dss	78-81	programmed cell death 1	Mus musculus	117-121
33036247-0	2020	The Antidiabetic Agent Acarbose Improves Anti-PD-1 and Rapamycin Efficacy in Preclinical Renal Cancer.	Acarbose	23-31	programmed cell death 1	Mus musculus	46-50
33117347-14	2020	In conclusion, the protective effects of T. spiralis AES on DSS-induced colitis were found to associate with PD-1 upregulation and M2 macrophage polarization.	dss	60-63	programmed cell death 1	Mus musculus	109-113
33020241-2	2020	Therefore, we aimed to study in vivo pharmacokinetics and whole-body distribution of zirconium-89 (89Zr) labeled programmed cell death protein-1 (PD-1) targeting pembrolizumab with positron-emission tomography (PET) in humanized mice.	Zirconium	85-94	programmed cell death 1	Mus musculus	113-144
33028694-7	2020	DMC combined with atezolizumab had more significant antitumor effect and stronger blocking effect on PD-1/PD-L1 pathway.	2,5-dimethylcelecoxib	0-3	programmed cell death 1	Mus musculus	101-105
33060147-10	2020	In situ vaccination of CMP-001 in combination with anti-PD-1 therapy induced durable tumor regression at injected and distant tumors and significantly prolonged mouse survival compared with anti-PD-1 therapy alone.	Cytidine Monophosphate	23-26	programmed cell death 1	Mus musculus	195-199
33060147-11	2020	The antitumor effect of CMP-001+anti-PD-1 was accompanied by increased interferon gamma (IFNgamma)+ CD4+/CD8+ T cells compared with control-treated mice.	Cytidine Monophosphate	24-27	programmed cell death 1	Mus musculus	37-41
33083737-0	2020	PD-1 Regulates GABAergic Neurotransmission and GABA-Mediated Analgesia and Anesthesia.	gamma-Aminobutyric Acid	15-19	programmed cell death 1	Mus musculus	0-4
33115945-7	2020	This study aimed to investigate whether cardiovascular adverse effects of the programmed cell death 1 (PD-1) inhibitor, a widely used ICI, were related to exosomal-transferred miR-34a-5p in cardiac senescence in a mouse model.	mir-34a-5p	176-186	programmed cell death 1	Mus musculus	78-101
33115945-7	2020	This study aimed to investigate whether cardiovascular adverse effects of the programmed cell death 1 (PD-1) inhibitor, a widely used ICI, were related to exosomal-transferred miR-34a-5p in cardiac senescence in a mouse model.	mir-34a-5p	176-186	programmed cell death 1	Mus musculus	103-107
32747421-4	2020	In this study we investigated the use of PBT to heighten therapeutic responses to PD-1 blockade in mice bearing 4T1 mammary carcinoma and B16F10 melanoma tumors.	(E)-2-(pent-3-en-1-yn-1-yl)thiophene	41-44	programmed cell death 1	Mus musculus	82-86
32747421-8	2020	PBT significantly enhanced the anti-tumor efficacy of PD-1 blockade in both 4T1 and B16F10 tumors resistant to anti-PD-1 monotherapy, increasing tumor-specific cytotoxic T-cells and survival of tumor-bearing animals beyond that with PBT or PD-1 blockade alone.	(E)-2-(pent-3-en-1-yn-1-yl)thiophene	0-3	programmed cell death 1	Mus musculus	54-58
32747421-8	2020	PBT significantly enhanced the anti-tumor efficacy of PD-1 blockade in both 4T1 and B16F10 tumors resistant to anti-PD-1 monotherapy, increasing tumor-specific cytotoxic T-cells and survival of tumor-bearing animals beyond that with PBT or PD-1 blockade alone.	(E)-2-(pent-3-en-1-yn-1-yl)thiophene	0-3	programmed cell death 1	Mus musculus	116-120
32747421-8	2020	PBT significantly enhanced the anti-tumor efficacy of PD-1 blockade in both 4T1 and B16F10 tumors resistant to anti-PD-1 monotherapy, increasing tumor-specific cytotoxic T-cells and survival of tumor-bearing animals beyond that with PBT or PD-1 blockade alone.	(E)-2-(pent-3-en-1-yn-1-yl)thiophene	0-3	programmed cell death 1	Mus musculus	116-120
32747421-8	2020	PBT significantly enhanced the anti-tumor efficacy of PD-1 blockade in both 4T1 and B16F10 tumors resistant to anti-PD-1 monotherapy, increasing tumor-specific cytotoxic T-cells and survival of tumor-bearing animals beyond that with PBT or PD-1 blockade alone.	(E)-2-(pent-3-en-1-yn-1-yl)thiophene	233-236	programmed cell death 1	Mus musculus	54-58
33115945-8	2020	METHODS AND RESULTS: The upregulation of miR-34a-5p in cardiomyocytes induced by exosomes derived from PD-1 inhibitor-treated macrophages, accompanied by cardiac senescence, caused cardiac injury in mouse hearts.	mir-34a-5p	41-51	programmed cell death 1	Mus musculus	103-107
32988398-11	2020	Pre-clinically, SB-3CT treatment enhanced the therapeutic efficacy of PD-1 or CTLA-4 blockade in the treatment of both primary and metastatic tumors.	SB 3CT compound	16-22	programmed cell death 1	Mus musculus	70-74
33046973-0	2020	Arsenic trioxide (ATO) induced degradation of Cyclin D1 sensitized PD-1/PD-L1 checkpoint inhibitor in oral and esophageal squamous cell carcinoma.	Arsenic Trioxide	0-16	programmed cell death 1	Mus musculus	67-71
33046973-0	2020	Arsenic trioxide (ATO) induced degradation of Cyclin D1 sensitized PD-1/PD-L1 checkpoint inhibitor in oral and esophageal squamous cell carcinoma.	Arsenic Trioxide	18-21	programmed cell death 1	Mus musculus	67-71
33083737-4	2020	Notably, GABA-induced currents in spinal dorsal horn neurons, thalamic neurons, and cortical neurons are suppressed by the PD-1-neutralizing immunotherapeutic Nivolumab in spinal cord slices, brain slices, and dissociated cortical neurons.	gamma-Aminobutyric Acid	9-13	programmed cell death 1	Mus musculus	123-127
33083737-5	2020	Reductions in GABA-mediated currents in CNS neurons were also observed in Pd1 -/- mice without changes in GABA receptor expression.	gamma-Aminobutyric Acid	14-18	programmed cell death 1	Mus musculus	74-77
33083737-7	2020	Finally, both GABA-mediated analgesia and anesthesia are impaired by Pd1 deficiency.	gamma-Aminobutyric Acid	14-18	programmed cell death 1	Mus musculus	69-72
32735004-4	2020	Most importantly, the Dox in the DDS can induce significant ICD while Sfn was able to remodel the TME, downregulate Treg, activate effector T cells and relieve programmed cell death protein 1 (PD-1) expression.	Doxorubicin	22-25	programmed cell death 1	Mus musculus	193-197
33455277-4	2020	Here, we report a biodegradable implant co-loaded with doxorubicin (DOX) and anti-PD-1 monoclonal antibody (aPD-1) (BI@DOX+aPD-1) for a combination of immunogenic chemotherapy and immune checkpoint therapy for PMC postoperative treatment.	Doxorubicin	119-122	programmed cell death 1	Mus musculus	82-86
33083737-8	2020	Our findings reveal PD-1 as a CNS-neuronal inhibitor that regulates GABAergic signaling and GABA-mediated behaviors.	gamma-Aminobutyric Acid	68-72	programmed cell death 1	Mus musculus	20-24
32432714-4	2020	Furthermore, combined treatment with anti-PD-1 and caspofungin resulted in a significant survival benefit compared with caspofungin or anti-PD-1 therapy alone, indicating a synergistic effect between PD-1-inhibitors and immunomodulatory antifungal agents.	Caspofungin	51-62	programmed cell death 1	Mus musculus	140-144
32908002-2	2020	Here, we report that increased amounts of histone 3 lysine 4 demethylase KDM5A in tumors markedly improved response to the treatment with the programmed cell death protein 1 (PD-1) antibody in mouse cancer models.	Lysine	52-58	programmed cell death 1	Mus musculus	142-173
32908002-2	2020	Here, we report that increased amounts of histone 3 lysine 4 demethylase KDM5A in tumors markedly improved response to the treatment with the programmed cell death protein 1 (PD-1) antibody in mouse cancer models.	Lysine	52-58	programmed cell death 1	Mus musculus	175-179
32943934-9	2020	Notably, moxibustion combined with paclitaxel inhibited the angiogenesis of tumors through the downregulation of CD34, HIF-1alpha, and VEGFA, and overcame the immunosuppressive microenvironment by inhibiting the PD-1/PD-L1 signaling pathway.	Paclitaxel	35-45	programmed cell death 1	Mus musculus	212-216
32983966-8	2020	Indeed, SAM+anti-PD-1 reversed the aberrant expression of some known melanoma genes.	S-Adenosylmethionine	8-12	programmed cell death 1	Mus musculus	17-21
32570034-9	2020	Further study showed that Gemcitabine treatment also increases CD8+ and CD4+ T cells proportion, PD-1 and PD-L1 expression in LLC mouse model.	gemcitabine	26-37	programmed cell death 1	Mus musculus	97-101
32814790-5	2020	Further, chronic morphine administration increases the numbers of circulating CD8+ T cells which express the inhibitory receptor PD-1, as well as the cytolytic proteins perforin and granzyme B in the infected mice.	Morphine	17-25	programmed cell death 1	Mus musculus	129-133
32430981-9	2020	Finally, mice that showed a good therapeutic response after the first cycle of immunization with the nanovaccine underwent a second cycle of immunization together with anti-PD-1 therapy, resulting in effective suppression of tumor relapse.	nanovaccine	101-112	programmed cell death 1	Mus musculus	173-177
32780726-2	2020	Here, we report that inhibiting palmitoyl-protein thioesterase 1 (PPT1), a target of CQ derivatives like hydroxychloroquine (HCQ), enhances the antitumor efficacy of anti-PD-1 Ab in melanoma.	Hydroxychloroquine	105-123	programmed cell death 1	Mus musculus	171-175
32780726-2	2020	Here, we report that inhibiting palmitoyl-protein thioesterase 1 (PPT1), a target of CQ derivatives like hydroxychloroquine (HCQ), enhances the antitumor efficacy of anti-PD-1 Ab in melanoma.	Hydroxychloroquine	125-128	programmed cell death 1	Mus musculus	171-175
32432714-4	2020	Furthermore, combined treatment with anti-PD-1 and caspofungin resulted in a significant survival benefit compared with caspofungin or anti-PD-1 therapy alone, indicating a synergistic effect between PD-1-inhibitors and immunomodulatory antifungal agents.	Caspofungin	51-62	programmed cell death 1	Mus musculus	140-144
32432714-4	2020	Furthermore, combined treatment with anti-PD-1 and caspofungin resulted in a significant survival benefit compared with caspofungin or anti-PD-1 therapy alone, indicating a synergistic effect between PD-1-inhibitors and immunomodulatory antifungal agents.	Caspofungin	120-131	programmed cell death 1	Mus musculus	42-46
32952954-7	2020	Results: Therapeutic combination of liposomal nanovaccine and CpG with anti PD-1 mAb, demonstrated the increased number of tumor infiltrated lymphocytes (TILs) in TME with the highest IFN-gamma production and cytotoxic activity, which led to remarkable tumor regression.	nanovaccine	46-57	programmed cell death 1	Mus musculus	76-80
32468061-0	2020	Recombinant programmed cell death 1 inhibits psoriatic inflammation in imiquimod-treated mice.	Imiquimod	71-80	programmed cell death 1	Mus musculus	12-35
32468061-6	2020	PD-1-fragment crystallizable (PD-1-Fc) treatment inhibited psoriatic inflammation and exhibited additive effects with anti-tumor necrosis factor alpha therapy in imiquimod-induced mouse psoriasis, suggesting that PD-1-Fc treatment may serve as a new therapeutic strategy for psoriasis.	Imiquimod	162-171	programmed cell death 1	Mus musculus	0-4
32468061-6	2020	PD-1-fragment crystallizable (PD-1-Fc) treatment inhibited psoriatic inflammation and exhibited additive effects with anti-tumor necrosis factor alpha therapy in imiquimod-induced mouse psoriasis, suggesting that PD-1-Fc treatment may serve as a new therapeutic strategy for psoriasis.	Imiquimod	162-171	programmed cell death 1	Mus musculus	30-34
32468061-6	2020	PD-1-fragment crystallizable (PD-1-Fc) treatment inhibited psoriatic inflammation and exhibited additive effects with anti-tumor necrosis factor alpha therapy in imiquimod-induced mouse psoriasis, suggesting that PD-1-Fc treatment may serve as a new therapeutic strategy for psoriasis.	Imiquimod	162-171	programmed cell death 1	Mus musculus	30-34
32952954-8	2020	Conclusion: Our results demonstrated the synergism between Lip-peptide+CpG nanovaccine and anti PD-1 regime, which improved the therapeutic efficacy of PD-1 checkpoint blocker in melanoma mice models.	lip-peptide	59-70	programmed cell death 1	Mus musculus	152-156
32952954-8	2020	Conclusion: Our results demonstrated the synergism between Lip-peptide+CpG nanovaccine and anti PD-1 regime, which improved the therapeutic efficacy of PD-1 checkpoint blocker in melanoma mice models.	nanovaccine	75-86	programmed cell death 1	Mus musculus	152-156
32819975-11	2020	The ability of FUS+GEM to control primary tumor outgrowth was moderately enhanced by either neoadjuvant or adjuvant treatment with anti-PD-1.	fusarubin	15-18	programmed cell death 1	Mus musculus	136-140
32691208-11	2020	Interestingly, treatment with selinexor and ibrutinib favored an anti-tumoral immune response by shifting polarization toward inflammatory M1-like and diminishing PD-1 and SIRPalpha expression in the remaining tumor-promoting M2-like macrophages.	selinexor	30-39	programmed cell death 1	Mus musculus	163-167
32691208-11	2020	Interestingly, treatment with selinexor and ibrutinib favored an anti-tumoral immune response by shifting polarization toward inflammatory M1-like and diminishing PD-1 and SIRPalpha expression in the remaining tumor-promoting M2-like macrophages.	ibrutinib	44-53	programmed cell death 1	Mus musculus	163-167
32819975-11	2020	The ability of FUS+GEM to control primary tumor outgrowth was moderately enhanced by either neoadjuvant or adjuvant treatment with anti-PD-1.	gemcitabine	19-22	programmed cell death 1	Mus musculus	136-140
32847988-10	2020	CDA induced rapid increase in immune regulatory pathways involving programmed death-1 (PD-1), indoleamine 2,3 dioxygenase (IDO) and cyclooxygenase-2 (COX2) in the TME.	cda	0-3	programmed cell death 1	Mus musculus	67-85
32847988-10	2020	CDA induced rapid increase in immune regulatory pathways involving programmed death-1 (PD-1), indoleamine 2,3 dioxygenase (IDO) and cyclooxygenase-2 (COX2) in the TME.	cda	0-3	programmed cell death 1	Mus musculus	87-91
32526602-7	2020	Consequently, combination with CDDP/PEM significantly enhanced the antitumor effects of anti-PD-1 antibody by decreasing numbers of intratumoral myeloid-derived suppressor cells (MDSCs) and vessels probably through suppression of VEGF expression by CDDP + PEM.	cddp/pem	31-39	programmed cell death 1	Mus musculus	93-97
32847988-11	2020	PD-1 blockade enhanced antitumor responses to CDA and increased mouse survival but mice did not eliminate primary tumor burdens.	cda	46-49	programmed cell death 1	Mus musculus	0-4
32526602-7	2020	Consequently, combination with CDDP/PEM significantly enhanced the antitumor effects of anti-PD-1 antibody by decreasing numbers of intratumoral myeloid-derived suppressor cells (MDSCs) and vessels probably through suppression of VEGF expression by CDDP + PEM.	Cisplatin	31-35	programmed cell death 1	Mus musculus	93-97
32923145-7	2020	tSNE analysis of the flow data revealed a resident phenotype of CD8+ T cells (PD-1+TIM-3+CTLA-4+) within untreated tumors, whereas DPX/CPA treatment induced recruitment of a novel population of CD8+ T cells (PD-1+TIM-3+CTLA-4-) within tumors.	Cyclophosphamide	135-138	programmed cell death 1	Mus musculus	208-212
32526602-7	2020	Consequently, combination with CDDP/PEM significantly enhanced the antitumor effects of anti-PD-1 antibody by decreasing numbers of intratumoral myeloid-derived suppressor cells (MDSCs) and vessels probably through suppression of VEGF expression by CDDP + PEM.	Pemetrexed	36-39	programmed cell death 1	Mus musculus	93-97
32526602-8	2020	CONCLUSIONS: The combination of anti-PD-1 antibody with CDDP + PEM may be a promising therapy for MPM via inhibiting the accumulation of MDSCs and vessels in tumors.	Pemetrexed	63-66	programmed cell death 1	Mus musculus	37-41
32426941-10	2020	Importantly, additional supplementation of L-arginine significantly increased the number of cured mice that were treated with CP and anti-PD-1 antibody.	Arginine	43-53	programmed cell death 1	Mus musculus	138-142
32655895-10	2020	AMG-232 potentiated tumor cell killing by T-cells in combination with anti-PD-1 antibody treatment, regardless of changes in PD-L1 expression.	2-(5-(3-chlorophenyl)-6-(4-chlorophenyl)-1-(1-(isopropylsulfonyl)-3-methylbutan-2-yl)-3-methyl-2-oxopiperidin-3-yl)acetic acid	0-7	programmed cell death 1	Mus musculus	75-79
32161121-0	2020	OMTX705, a Novel FAP-Targeting ADC demonstrates Activity in Chemotherapy and PD1-Resistant Solid Tumors Models.	omtx705	0-7	programmed cell death 1	Mus musculus	77-80
32342332-5	2020	We investigated the use of a PP2A inhibitor, LB-100, to enhance antitumor efficacy of PD1 blockade in a syngeneic glioma model.	lb100	45-51	programmed cell death 1	Mus musculus	86-89
32078015-8	2020	In addition, IBI101 shows efficacious anti-tumor activity in mice when administrated alone or in combination with anti-PD-1 antibodies.	ibi101	13-19	programmed cell death 1	Mus musculus	119-123
32078015-9	2020	In human OX40 knock-in mice bearing MC38 colon carcinoma, IBI101 treatment induces tumor antigen-specific CD8+ T-cell responses, decreases immunosuppressive regulatory T cells in tumor, and enhances the immune response to PD-1 inhibition.	ibi101	58-64	programmed cell death 1	Mus musculus	222-226
32923114-9	2020	Conclusions: The correlation between ROS1-fusion and PD-L1 overexpression suggested that PD-L1/PD-1 blockade could be the second-line treatment option for the Crizotinib-resistant NSCLC with ROS1 rearrangement.	Crizotinib	159-169	programmed cell death 1	Mus musculus	95-99
32245889-4	2020	PRMT1 deletion in mice reduced PD-L1 and PD-L2 expression in tumors and reduced the efficiency of PD-1 antibody treatment in a diethylnitrosamine-induced HCC mouse model, suggesting that PRMT1 regulates the hepatic immune checkpoint.	Diethylnitrosamine	127-145	programmed cell death 1	Mus musculus	98-102
32017146-2	2020	(a) Ho et al administered GAP (anti-GITR, IFN-alpha, anti-PD1 with localized radiation) to treat 4T1 murine breast carcinoma with complete tumor eradication in 50% of treated mice, (b) Sallets et al treated murine B-Lymphoma with anti-GITR, localized intratumoral injection of STING agonist (whose downstream molecule is type I IFN) and anti-PD1, and achieved 50% complete tumor eradication, and (c) Schoenhals et al treated murine non-small cell lung carcinoma with anti-GITR, anti-PD1 and localized radiation (which they had previously demonstrated radiation mediated Type I IFN dependent mechanism was important for anti-PD1 treatment), and obtained 60% complete eradication.	Holmium	4-6	programmed cell death 1	Mus musculus	58-61
32448803-11	2020	Captopril treatment also increased the expression of checkpoint receptor PD-1 on CD8+and DNT subsets .	Captopril	0-9	programmed cell death 1	Mus musculus	73-77
32017146-2	2020	(a) Ho et al administered GAP (anti-GITR, IFN-alpha, anti-PD1 with localized radiation) to treat 4T1 murine breast carcinoma with complete tumor eradication in 50% of treated mice, (b) Sallets et al treated murine B-Lymphoma with anti-GITR, localized intratumoral injection of STING agonist (whose downstream molecule is type I IFN) and anti-PD1, and achieved 50% complete tumor eradication, and (c) Schoenhals et al treated murine non-small cell lung carcinoma with anti-GITR, anti-PD1 and localized radiation (which they had previously demonstrated radiation mediated Type I IFN dependent mechanism was important for anti-PD1 treatment), and obtained 60% complete eradication.	Holmium	4-6	programmed cell death 1	Mus musculus	342-345
32017146-2	2020	(a) Ho et al administered GAP (anti-GITR, IFN-alpha, anti-PD1 with localized radiation) to treat 4T1 murine breast carcinoma with complete tumor eradication in 50% of treated mice, (b) Sallets et al treated murine B-Lymphoma with anti-GITR, localized intratumoral injection of STING agonist (whose downstream molecule is type I IFN) and anti-PD1, and achieved 50% complete tumor eradication, and (c) Schoenhals et al treated murine non-small cell lung carcinoma with anti-GITR, anti-PD1 and localized radiation (which they had previously demonstrated radiation mediated Type I IFN dependent mechanism was important for anti-PD1 treatment), and obtained 60% complete eradication.	Holmium	4-6	programmed cell death 1	Mus musculus	342-345
32230980-2	2020	Our previous study showed that dual PI3K/mTOR inhibitor Dactolisib impaired the viability and immunosuppressive function of Gr-MDSCs, and significantly synergized with immune checkpoint blockade (ICB) antibodies targeting PD1 and CTLA4 to eradicate metastatic castration-resistant prostate cancer (CRPC) in a preclinical transgenic mouse model.	dactolisib	56-66	programmed cell death 1	Mus musculus	222-225
32425919-5	2020	After PD-1 antibody treatment, the injection of antibiotics counteracted the efficacy of PD-1 antibody in inhibiting tumor growth when compared with the Control group (mice were treated with sterile drinking water).	Water	208-213	programmed cell death 1	Mus musculus	89-93
32425919-9	2020	Changes in gut microbiome leaded to changes in glycerophospholipid metabolism level, which may affect the expression of immune-related cytokines IFN-gamma and IL-2 in the tumor microenvironment, resulting in a different therapeutic effect of PD-1 antibody.	Glycerophospholipids	47-66	programmed cell death 1	Mus musculus	242-246
32425919-10	2020	Our findings show that changes in the gut microbiome affect the glycerophospholipid metabolic pathway, thereby regulating the therapeutic potential of PD-1 antibody in the immunotherapy of MSS-type CRC tumor-bearing mice.	Glycerophospholipids	64-83	programmed cell death 1	Mus musculus	151-155
32332730-4	2020	Alcohol-exposed mice have reduced Bcl6 and PD-1 expression as well as IL-21 production by TFH cells, preventing proper spatial organization of TFH cells to form TFH:B cell conjugates in germinal centers.	Alcohols	0-7	programmed cell death 1	Mus musculus	43-47
32368288-5	2020	In this study, we have shown that CG-745 induces microenvironment changes promoting anti-cancer effect of anti-PD-1 antibody in syngeneic mouse models.	UNII-QA3Y8EZG57	34-40	programmed cell death 1	Mus musculus	111-115
32292786-9	2020	Additionally, we found that AAV-IL-27 local therapy had significant synergy with anti-PD-1 or T cell adoptive transfer therapy.	CHEMBL2031461	28-31	programmed cell death 1	Mus musculus	86-90
32494661-5	2020	Combining Vps34i improved the therapeutic benefit of anti-PD-L1/PD-1 in melanoma and CRC and prolonged mice survival.	vps34i	10-16	programmed cell death 1	Mus musculus	64-68
32215185-9	2020	AZD8186 significantly enhanced antitumor efficacy of anti-PD1 antibodies in the PTEN-deficient BP murine melanoma xenograft model, but not in the PTEN-wild-type CT26 xenograft model.	AZD8186	0-7	programmed cell death 1	Mus musculus	58-61
32189078-2	2020	We previously reported that anti-PD-1 treatment affected tumor glycolysis by using 2-deoxy-2-[18F]fluoro-D-glucose ([18F]FDG) positron emission tomography (PET).	Fluorodeoxyglucose F18	83-114	programmed cell death 1	Mus musculus	33-37
32189078-11	2020	The cGAMP/anti-PD-1 combination group had significantly lower levels of GLUT1high cells/hexokinase IIhigh cells in CD45- cancer cells compared with tumors in the anti-PD-1 treated group.	cyclic guanosine monophosphate-adenosine monophosphate	4-9	programmed cell death 1	Mus musculus	15-19
32189078-11	2020	The cGAMP/anti-PD-1 combination group had significantly lower levels of GLUT1high cells/hexokinase IIhigh cells in CD45- cancer cells compared with tumors in the anti-PD-1 treated group.	cyclic guanosine monophosphate-adenosine monophosphate	4-9	programmed cell death 1	Mus musculus	167-171
32189078-13	2020	Such a change of glucose uptake might be caused by the difference in infiltration or activation level of immune cells between the anti-PD-1 treated group and the cGAMP/anti-PD-1 combination group.	Glucose	17-24	programmed cell death 1	Mus musculus	135-139
32215185-15	2020	However, AZD8186 has enhanced efficacy when combined with paclitaxel and anti-PD1 in vivo.	AZD8186	9-16	programmed cell death 1	Mus musculus	78-81
32088639-11	2020	Finally, the anti-PD-1 plus DNA hypomethylating agent azacytidine could significantly suppressed the tumor growth better than the anti-PD-1 therapy.	Azacitidine	54-65	programmed cell death 1	Mus musculus	135-139
31640402-9	2020	The mRNA levels of PD-L1 and PD-1 were significantly elevated 2 h, 4 h and 6 h after acute nitroglycerin treatment (p &lt; 0.05).	Nitroglycerin	91-104	programmed cell death 1	Mus musculus	29-33
31640402-10	2020	The protein levels of PD-L1 were significantly increased 2 h, 4 h and 6 h after treatment, and PD-1 was significantly increased at 2 h and 6 h. The blockade of PD-1 increased acute nitroglycerin-induced hyperalgesia, and this effect was accompanied by a more significant increase in calcitonin gene-related peptide, IL-1beta, TNF-alpha, IL-6 and IL-18 in the trigeminal ganglia.	Nitroglycerin	181-194	programmed cell death 1	Mus musculus	95-99
31640402-10	2020	The protein levels of PD-L1 were significantly increased 2 h, 4 h and 6 h after treatment, and PD-1 was significantly increased at 2 h and 6 h. The blockade of PD-1 increased acute nitroglycerin-induced hyperalgesia, and this effect was accompanied by a more significant increase in calcitonin gene-related peptide, IL-1beta, TNF-alpha, IL-6 and IL-18 in the trigeminal ganglia.	Nitroglycerin	181-194	programmed cell death 1	Mus musculus	160-164
32274726-5	2020	Pixatimod has been tested in combination with a number of approved anti-cancer drugs demonstrating its clinical potential, including with gemcitabine, paclitaxel, sorafenib, platinum agents and an anti-PD-1 antibody.	PG 545	0-9	programmed cell death 1	Mus musculus	202-206
32075945-5	2020	Here, we report that morphine antinociception and MOR signaling require neuronal PD-1.	Morphine	21-29	programmed cell death 1	Mus musculus	81-85
32075945-6	2020	Morphine-induced antinociception after systemic or intrathecal injection was compromised in Pd1 -/- mice.	Morphine	0-8	programmed cell death 1	Mus musculus	92-95
32075945-7	2020	Morphine antinociception was also diminished in wild-type mice after intravenous or intrathecal administration of nivolumab, a clinically used anti-PD-1 monoclonal antibody.	Morphine	0-8	programmed cell death 1	Mus musculus	148-152
32075945-8	2020	In mouse models of inflammatory, neuropathic, and cancer pain, spinal morphine antinociception was compromised in Pd1 -/- mice.	Morphine	70-78	programmed cell death 1	Mus musculus	114-117
32075945-10	2020	Morphine produced antinociception by (i) suppressing calcium currents in DRG neurons, (ii) suppressing excitatory synaptic transmission, and (iii) inducing outward currents in spinal cord neurons; all of these actions were impaired by PD-1 blockade in mice.	Morphine	0-8	programmed cell death 1	Mus musculus	235-239
31978106-0	2020	The inhibitor of apoptosis proteins antagonist Debio 1143 promotes the PD-1 blockade-mediated HIV load reduction in blood and tissues of humanized mice.	N-benzhydryl-5-(2-(methylamino)propanamido)-3-(3-methylbutanoyl)-6-oxodecahydropyrrolo(1,2-a)(1,5)diazocine-8-carboxamide	47-57	programmed cell death 1	Mus musculus	71-75
31451071-0	2020	PGC-1alpha activator-induced fatty acid oxidation in tumor-infiltrating CTLs enhances effects of PD-1 blockade therapy in lung cancer.	Fatty Acids	29-39	programmed cell death 1	Mus musculus	97-101
31806638-8	2020	The antitumor effectiveness of anti-PD1 was abolished in TDO-KO mice fed with a tryptophan-low diet that normalized their blood tryptophan level.	Tryptophan	80-90	programmed cell death 1	Mus musculus	36-39
31806638-8	2020	The antitumor effectiveness of anti-PD1 was abolished in TDO-KO mice fed with a tryptophan-low diet that normalized their blood tryptophan level.	Tryptophan	128-138	programmed cell death 1	Mus musculus	36-39
32405624-13	2019	Conclusions: The addition of anti-PD1 antibody with GVAX and/or anti-CSF-1R antibody to gemcitabine improved the survival of mice with liver-metastatic pancreatic ductal adenocarcinoma (PDA).	gvax	52-56	programmed cell death 1	Mus musculus	34-37
31506388-0	2019	Cisplatin Facilitates Radiation-Induced Abscopal Effects in Conjunction with PD-1 Checkpoint Blockade Through CXCR3/CXCL10-Mediated T-cell Recruitment.	Cisplatin	0-9	programmed cell death 1	Mus musculus	77-81
31651174-0	2019	PLGA Nanoparticles Co-Delivering siRNAs against Programmed Cell Death Protein-1 and Its Ligand Gene for Suppression of Colon Tumor Growth.	plga	0-4	programmed cell death 1	Mus musculus	48-79
31651174-4	2019	Here, we simultaneously silenced PD-1 and PD-L1 expression on CTLs and colon tumors using PD-1 siRNA/PD-L1 siRNA-loaded PLGA nanoparticles and investigated functional activation of tumor-specific CTLs.	plga	120-124	programmed cell death 1	Mus musculus	90-94
31651174-7	2019	Ultimately, systemic administration of PD-1 and PD-L1 siRNA via PLGA nanoparticles restored the effector functions of tumor-specific CTLs in MC38 tumor-bearing mice.	plga	64-68	programmed cell death 1	Mus musculus	39-43
31409612-3	2019	The approval of pemetrexed and carboplatin with anti-PD-1 (pembrolizumab) for treatment of non-small cell lung cancer represents the first approved chemotherapy and immunotherapy combination.	Pemetrexed	16-26	programmed cell death 1	Mus musculus	53-57
31409612-9	2019	CONCLUSIONS: Pemetrexed augments systemic intratumor immune responses through tumor intrinsic mechanisms including immunogenic cell death, T-cell-intrinsic mechanisms enhancing mitochondrial biogenesis leading to increased T-cell infiltration/activation along with modulation of innate immune pathways, which are significantly enhanced in combination with PD-1 pathway blockade.See related commentary by Buque et al., p. 6890.	Pemetrexed	13-23	programmed cell death 1	Mus musculus	356-360
31358531-4	2019	Inhibition of PCs in T cells using the general protein-based inhibitor alpha1-PDX or the pharmacological inhibitor Decanoyl-Arg-Val-Lys-Arg-chloromethylketone (CMK) repressed PD-1 and exhaustion of CTLs via induction of T-cell proliferation and apoptosis inhibition, which improved CTL efficacy against microsatellite instable (MSI) and stable (MSS) colon cancer cells.	decanoyl-arg-val-lys-arg	115-139	programmed cell death 1	Mus musculus	175-179
31727535-4	2021	RESULTS: The CLP sepsis model induced AKI in C57/B6 mice; The expression of PD-1 and PD-L1 were increased in septic AKI mice; PD-1/PD-L1 induced apoptosis in T cells: the number of lymphocytes decreased by 64%, while the number of CD3+ T cells decreased by 27% compared with the sham group; Results also indicated that lactate up-regulates expression of PD-L1 in the kidney.	Lactic Acid	319-326	programmed cell death 1	Mus musculus	76-80
31727535-5	2021	CONCLUSIONS: Lactate activated PD-1/PD-L1 pathway can induce immunosuppression by inducing apoptosis in lymphocytes in septic AKI.	Lactic Acid	13-20	programmed cell death 1	Mus musculus	31-35
31358531-4	2019	Inhibition of PCs in T cells using the general protein-based inhibitor alpha1-PDX or the pharmacological inhibitor Decanoyl-Arg-Val-Lys-Arg-chloromethylketone (CMK) repressed PD-1 and exhaustion of CTLs via induction of T-cell proliferation and apoptosis inhibition, which improved CTL efficacy against microsatellite instable (MSI) and stable (MSS) colon cancer cells.	chloromethylketone	140-158	programmed cell death 1	Mus musculus	175-179
31408442-7	2019	Furthermore, teniposide potentiated the antitumor efficacy of anti-PD1 on multiple types of mouse tumor models.	Teniposide	13-23	programmed cell death 1	Mus musculus	67-70
31437792-5	2019	Both baicalein and baicalin enhanced the cytotoxicity of T cells to eliminate tumor cells, which was abrogated after HCC cells were transfected with a PD-L1 overexpression plasmid or after T cells were pretreated with an anti-PD-1 blocking antibody.	baicalein	5-14	programmed cell death 1	Mus musculus	226-230
31437792-5	2019	Both baicalein and baicalin enhanced the cytotoxicity of T cells to eliminate tumor cells, which was abrogated after HCC cells were transfected with a PD-L1 overexpression plasmid or after T cells were pretreated with an anti-PD-1 blocking antibody.	baicalin	19-27	programmed cell death 1	Mus musculus	226-230
31429085-0	2019	Upregulation of PD-1 follows tumour development in the AOM/DSS model of inflammation-induced colorectal cancer in mice.	dss	59-62	programmed cell death 1	Mus musculus	16-20
31429085-10	2019	Blocking PD-1 signalling with an anti-PD1 antibody did not affect the tumour burden in the AOM/DSS-treated mice, but did potentiate the weight loss in the third DSS cycle, indicating possible immune-mediated toxicity.	dss	161-164	programmed cell death 1	Mus musculus	9-13
31462297-0	2019	Prim-O-glucosylcimifugin enhances the antitumour effect of PD-1 inhibition by targeting myeloid-derived suppressor cells.	prim-O-glucosylcimifugin	0-24	programmed cell death 1	Mus musculus	59-63
31408442-8	2019	Our findings showed that teniposide could trigger tumor immunogenicity, and enabled a potential chemo-immunotherapeutic approach to potentiate the therapeutic efficacy of anti-PD1 immunotherapy.	Teniposide	25-35	programmed cell death 1	Mus musculus	176-179
29665659-1	2018	4-Hydroxy-2-(4-hydroxyphenethyl)isoindoline-1,3-dione (PD1) is a synthetic phthalimide derivative of a marine compound.	4-hydroxy-2-(4-hydroxyphenethyl)isoindoline-1,3-dione	0-53	programmed cell death 1	Mus musculus	55-58
31291983-3	2019	METHODS: Anti-PD-1 antibody was administered in the 4NQO-induced carcinogenesis mouse models.	4-Nitroquinoline-1-oxide	52-56	programmed cell death 1	Mus musculus	14-18
30910830-6	2019	Administration of the SIRT1 inhibitor sirtinol (10 mg/kg body weight) in infected mice decreased spleen parasite burden and a synergistic effect was found with PD-1 inhibitor.	sirtinol	38-46	programmed cell death 1	Mus musculus	160-164
30382588-8	2019	In addition, CD8 expression was increased while OCT4&amp;SOX2 expressions were decreased in OCT4&amp;SOX2 CTLs + PD-1 inhibitor group than OCT4&amp;SOX2 CTLs group and PD-1 inhibitor group.	Adenosine Monophosphate	53-56	programmed cell death 1	Mus musculus	113-117
29622799-4	2019	A more significant inhibition of tumor growth and a prolongation of survival were observed in the CT26 mouse model after treatment with a combination of PD-1 blockade and decitabine than in mice treated with decitabine or PD-1 blockade alone.	Decitabine	171-181	programmed cell death 1	Mus musculus	222-226
29622799-4	2019	A more significant inhibition of tumor growth and a prolongation of survival were observed in the CT26 mouse model after treatment with a combination of PD-1 blockade and decitabine than in mice treated with decitabine or PD-1 blockade alone.	Decitabine	208-218	programmed cell death 1	Mus musculus	153-157
29622799-5	2019	The anti-tumor effect of the PD-1 blockade was enhanced by low-dose decitabine.	Decitabine	68-78	programmed cell death 1	Mus musculus	29-33
29622799-7	2019	Therefore, decitabine-based tumor microenvironment re-modulation could improve the effect of the PD-1 blockade.	Decitabine	11-21	programmed cell death 1	Mus musculus	97-101
30760618-5	2019	When PD-1 is inhibited, both in vitro and in vivo, the efficacy of BT-11 is reduced, validating this assertion.	BT-11	67-72	programmed cell death 1	Mus musculus	5-9
30934955-2	2019	We have recently reported that programmed cell death protein-1 (PD-1) ligand (PD-L1) expression is regulated by lactate present at high levels in the tumor microenvironment (TME).	Lactic Acid	112-119	programmed cell death 1	Mus musculus	31-62
30948928-0	2019	Lycopene improves the efficiency of anti-PD-1 therapy via activating IFN signaling of lung cancer cells.	Lycopene	0-8	programmed cell death 1	Mus musculus	41-45
30948928-2	2019	In this study, we aimed to investigate whether lycopene could promote the effect of anti-PD-1 treatment on lung cancer.	Lycopene	47-55	programmed cell death 1	Mus musculus	89-93
30948928-8	2019	Cell apoptosis in the tumor tissues was significantly enhanced in mice with combined lycopene and anti-PD-1 treatment in comparison with those of either lycopene or anti-PD-1 alone.	Lycopene	85-93	programmed cell death 1	Mus musculus	170-174
30948928-9	2019	Furthermore, lycopene could assist anti-PD-1 to elevate the levels of interleukin (IL)-1 and interferon (IFN) gamma while reduce the levels of IL-4 and IL-10 in the spleen of mice injected with LLC cells.	Lycopene	13-21	programmed cell death 1	Mus musculus	40-44
30948928-12	2019	Conclusion: Our results have demonstrated that lycopene could be used as a potential adjuvant drug to synergistically improve the efficiency of anti-PD-1 therapy.	Lycopene	47-55	programmed cell death 1	Mus musculus	149-153
30547218-8	2019	Indeed, Belinostat combined with the simultaneous blockade of CTLA-4 and PD-1 led to complete tumor rejection.	belinostat	8-18	programmed cell death 1	Mus musculus	73-77
30609280-8	2019	Thus, our results identified a potentially novel mechanism of the therapeutic action of indirubin in the treatment of ITP through regulating the homeostasis of CD4+ T cells in a PD1/PTEN/AKT signalling pathway.	indirubin	88-97	programmed cell death 1	Mus musculus	178-181
30910561-7	2019	Contact residues, shown to be critical for binding of the respective human and murine PD-1 ligands are mostly conserved between avian and mammalian species, whereas residues that define the cytoplasmic immunoreceptor tyrosine-based inhibitory motif (ITIM) and immunoreceptor tyrosine-based switch motif (ITSM) are highly conserved across higher vertebrates and frog.	Tyrosine	217-225	programmed cell death 1	Mus musculus	86-90
30910561-7	2019	Contact residues, shown to be critical for binding of the respective human and murine PD-1 ligands are mostly conserved between avian and mammalian species, whereas residues that define the cytoplasmic immunoreceptor tyrosine-based inhibitory motif (ITIM) and immunoreceptor tyrosine-based switch motif (ITSM) are highly conserved across higher vertebrates and frog.	Tyrosine	275-283	programmed cell death 1	Mus musculus	86-90
30565657-5	2019	Moreover, STDENVANT upregulated programmed death 1 (PD-1) and its ligand PD-L1 on effector T cells, DCs, and glioma tissues, resulting in the accumulation of regulatory T (Treg) cells in the brain and lymph nodes.	stdenvant	10-19	programmed cell death 1	Mus musculus	32-50
30565657-5	2019	Moreover, STDENVANT upregulated programmed death 1 (PD-1) and its ligand PD-L1 on effector T cells, DCs, and glioma tissues, resulting in the accumulation of regulatory T (Treg) cells in the brain and lymph nodes.	stdenvant	10-19	programmed cell death 1	Mus musculus	52-56
30791466-9	2019	JA-0009 showed limited sensitivity when treated with antibodies against inhibitory checkpoint molecules (anti-mPD-1 and anti-mCTLA-4), but high sensitivity to gemcitabine treatment.	ja-0009	0-7	programmed cell death 1	Mus musculus	110-115
30755715-0	2019	Niraparib activates interferon signaling and potentiates anti-PD-1 antibody efficacy in tumor models.	niraparib	0-9	programmed cell death 1	Mus musculus	62-66
30736857-10	2019	Humanized mice treated with anti-PD-1 exhibited increased anti-tumor human T-cell responses coupled with decreased Treg and myeloid populations that correlated with tumor growth inhibition.	treg	115-119	programmed cell death 1	Mus musculus	33-37
30431333-10	2019	NEW &amp; NOTEWORTHY Our study shows not only that ligands of the checkpoint protein PD-1 respond inversely to a stressor such as septic challenge (PD-L2 declines, whereas PD-L1 rises) but also that aspects of liver dysfunction increase in septic mice lacking the PD-L2 gene.	Adenosine Monophosphate	5-8	programmed cell death 1	Mus musculus	85-89
30142009-8	2019	The combination of [sorafenib + vorinostat] with an anti-PD-1 antibody caused a significant further reduction in tumor growth compared to the drug combination alone.	Sorafenib	20-29	programmed cell death 1	Mus musculus	57-61
30142009-8	2019	The combination of [sorafenib + vorinostat] with an anti-PD-1 antibody caused a significant further reduction in tumor growth compared to the drug combination alone.	Vorinostat	32-42	programmed cell death 1	Mus musculus	57-61
30095976-9	2018	Together, these data demonstrate that PD-1/PD-L1-mediated immunosuppression may occur in LAM, and suggest new opportunities for therapeutic targeting that may provide benefits beyond those of rapamycin.	Sirolimus	192-201	programmed cell death 1	Mus musculus	38-42
30481959-8	2018	Not only does the DOX/IND-Liposome provide a synergistic antitumor response that is superior to a DOX-only liposome, but it also demonstrated that the carrier could be effectively combined with PD-1 blocking antibodies to eradicate lung metastases.	Doxorubicin	18-21	programmed cell death 1	Mus musculus	194-198
30481959-8	2018	Not only does the DOX/IND-Liposome provide a synergistic antitumor response that is superior to a DOX-only liposome, but it also demonstrated that the carrier could be effectively combined with PD-1 blocking antibodies to eradicate lung metastases.	1-methyltryptophan	22-25	programmed cell death 1	Mus musculus	194-198
29665659-1	2018	4-Hydroxy-2-(4-hydroxyphenethyl)isoindoline-1,3-dione (PD1) is a synthetic phthalimide derivative of a marine compound.	phthalimide	75-86	programmed cell death 1	Mus musculus	55-58
29938495-7	2018	There was a significant increase in ALT in PD-1-/- mice co-treated with anti-LAG3 or anti-TGF-beta relative to AQ-treated wild-type mice.	Amodiaquine	111-113	programmed cell death 1	Mus musculus	43-47
30172698-2	2018	In a previous study, we found that the addition of metformin to nivolumab, an anti-programmed cell death protein 1 (PD-1) antibody, yielded substantial tumor regression in mouse models.	Metformin	51-60	programmed cell death 1	Mus musculus	83-114
30172698-2	2018	In a previous study, we found that the addition of metformin to nivolumab, an anti-programmed cell death protein 1 (PD-1) antibody, yielded substantial tumor regression in mouse models.	Metformin	51-60	programmed cell death 1	Mus musculus	116-120
28479601-4	2018	More than a decade ago, we reported that replacement of a murine B7-DC mutant lysine with serine (K113S) at positive 113 resulted in a loss of binding capacity to PD-1.	Lysine	78-84	programmed cell death 1	Mus musculus	163-167
28479601-4	2018	More than a decade ago, we reported that replacement of a murine B7-DC mutant lysine with serine (K113S) at positive 113 resulted in a loss of binding capacity to PD-1.	Serine	90-96	programmed cell death 1	Mus musculus	163-167
29948678-3	2018	Mice of lycopene group were gavaged with 20 mg/kg/day lycopene from PD1 to PD7 and then given 500 mg/kg/day BPA from PD8 to PD14.	Lycopene	8-16	programmed cell death 1	Mus musculus	68-71
29948678-3	2018	Mice of lycopene group were gavaged with 20 mg/kg/day lycopene from PD1 to PD7 and then given 500 mg/kg/day BPA from PD8 to PD14.	Lycopene	54-62	programmed cell death 1	Mus musculus	68-71
29455288-0	2018	Mycophenolate Mofetil Protects Septic Mice via the Dual Inhibition of Inflammatory Cytokines and PD-1.	Mycophenolic Acid	0-21	programmed cell death 1	Mus musculus	97-101
29609517-0	2018	PD-1 Inhibition Minimally Affects Cisplatin-Induced Toxicities in a Murine Model.	Cisplatin	34-43	programmed cell death 1	Mus musculus	0-4
29609517-2	2018	The impact of anti-PD-1 therapy on cisplatin-induced ototoxicity and nephrotoxicity has not been established.	Cisplatin	35-44	programmed cell death 1	Mus musculus	19-23
29556048-12	2018	Addition of ADT to anti-PD1 therapy and cryoablation doubled the time to accelerated growth in the untreated tumors (p = 0.0021) and extended survival when compared to cryoablation combined with ADT in 25% of the mice.	adt	12-15	programmed cell death 1	Mus musculus	24-27
29618655-7	2018	AAV-IL-27 also dramatically increased the efficacy of anti-PD-1 therapy, presumably due to induction of PD-L1 in T cells and depletion of Tregs.	tregs	138-143	programmed cell death 1	Mus musculus	59-63
29643229-6	2018	Combination of anti-PD1 and anti-CSF1 receptor (CSF1R) antibodies induced the regression of BRAFV600E -driven, transplant mouse melanomas, a result that was dependent on the effective elimination of TAMs.	tams	199-203	programmed cell death 1	Mus musculus	20-23
29337311-0	2018	Dinaciclib induces immunogenic cell death and enhances anti-PD1-mediated tumor suppression.	dinaciclib	0-10	programmed cell death 1	Mus musculus	60-63
28633555-0	2018	Glutamine Administration in Early or Late Septic Phase Downregulates Lymphocyte PD-1/PD-L1 Expression and the Inflammatory Response in Mice With Polymicrobial Sepsis.	Glutamine	0-9	programmed cell death 1	Mus musculus	80-84
28633555-3	2018	This study administered glutamine (GLN) in the early or late phase of sepsis to investigate its effects on regulating leukocyte programmed cell death 1 (PD-1) and its ligand (programmed cell death ligand 1 [PD-L1]) expression, macrophage function, inflammation, and acute kidney injury in sepsis.	Glutamine	24-33	programmed cell death 1	Mus musculus	153-157
28633555-3	2018	This study administered glutamine (GLN) in the early or late phase of sepsis to investigate its effects on regulating leukocyte programmed cell death 1 (PD-1) and its ligand (programmed cell death ligand 1 [PD-L1]) expression, macrophage function, inflammation, and acute kidney injury in sepsis.	Glutamine	35-38	programmed cell death 1	Mus musculus	153-157
28633555-9	2018	GLN administration decreased plasma IL-6 level, downregulated the percentage of IL-17A-expressing CD4+ T cells, attenuated macrophage dysfunction, decreased caspase-3 mRNA expression, and reduced PD-1/PD-L1 expression by T and B cells.	Glutamine	0-3	programmed cell death 1	Mus musculus	196-200
28633555-11	2018	GLN administered at 3 and 10 hours after CLP offered nearly equal effects on PD-1/PD-L1 and inflammatory mediator expression after CLP.	Glutamine	0-3	programmed cell death 1	Mus musculus	77-81
29337311-5	2018	Dinaciclib induced a type I IFN gene signature within the tumor, leading us to hypothesize that dinaciclib potentiates the effects of anti-PD1 by eliciting ICD.	dinaciclib	0-10	programmed cell death 1	Mus musculus	139-142
29337311-5	2018	Dinaciclib induced a type I IFN gene signature within the tumor, leading us to hypothesize that dinaciclib potentiates the effects of anti-PD1 by eliciting ICD.	dinaciclib	96-106	programmed cell death 1	Mus musculus	139-142
29337311-8	2018	These findings identify a potential mechanism for the observed benefit of combining dinaciclib and anti-PD1, in which dinaciclib induces ICD, thereby converting the tumor cell into an endogenous vaccine and boosting the effects of anti-PD1.	dinaciclib	84-94	programmed cell death 1	Mus musculus	236-239
29337311-8	2018	These findings identify a potential mechanism for the observed benefit of combining dinaciclib and anti-PD1, in which dinaciclib induces ICD, thereby converting the tumor cell into an endogenous vaccine and boosting the effects of anti-PD1.	dinaciclib	118-128	programmed cell death 1	Mus musculus	104-107
29337311-8	2018	These findings identify a potential mechanism for the observed benefit of combining dinaciclib and anti-PD1, in which dinaciclib induces ICD, thereby converting the tumor cell into an endogenous vaccine and boosting the effects of anti-PD1.	dinaciclib	118-128	programmed cell death 1	Mus musculus	236-239
29016938-8	2018	A higher percentage of long-term survivors was observed in mice treated with combined GMCI/anti-PD-1 relative to single treatments.	gmci	86-90	programmed cell death 1	Mus musculus	96-100
29087505-5	2018	PD1-/- mice treated with anti-CTLA-4 and troglitazone or tolcapone displayed liver injury as determined by ALT levels and histology, while pioglitazone and entacapone showed less signs of liver injury.	Troglitazone	41-53	programmed cell death 1	Mus musculus	0-3
29087505-5	2018	PD1-/- mice treated with anti-CTLA-4 and troglitazone or tolcapone displayed liver injury as determined by ALT levels and histology, while pioglitazone and entacapone showed less signs of liver injury.	Tolcapone	57-66	programmed cell death 1	Mus musculus	0-3
29016938-12	2018	Our data suggest that anti-PD-1 treatment improves the effectiveness of GMCI by overcoming interferon-induced PD-L1-mediated inhibitory signals, and GMCI improves anti-PD-1 efficacy by increasing tumor-infiltrating T-cell activation.	gmci	72-76	programmed cell death 1	Mus musculus	27-31
29016938-12	2018	Our data suggest that anti-PD-1 treatment improves the effectiveness of GMCI by overcoming interferon-induced PD-L1-mediated inhibitory signals, and GMCI improves anti-PD-1 efficacy by increasing tumor-infiltrating T-cell activation.	gmci	149-153	programmed cell death 1	Mus musculus	168-172
29016938-13	2018	Conclusions: Our data show that the GMCI/anti-PD-1 combination is well tolerated and effective in glioblastoma mouse models.	gmci	36-40	programmed cell death 1	Mus musculus	46-50
29123953-4	2017	Here, we report for the first time effects of PD-1 blockade on ch14.18/CHO-based immunotherapy and mechanisms involved.	CAV protocol	71-74	programmed cell death 1	Mus musculus	46-50
29149031-2	2017	This study was conducted both in vitro and in vivo on the ethyl acetate extract (PD1) of farmed red macroalgae in order to explore its anti-inflammatory properties.	ethyl acetate	58-71	programmed cell death 1	Mus musculus	81-84
29149031-4	2017	For evaluating the potential in vivo anti-inflammatory and antinociceptive effects of PD1, we used carrageenan-induced rat paw edema to produce inflammatory pain.	Carrageenan	99-110	programmed cell death 1	Mus musculus	86-89
29149031-6	2017	Oral PD1 can reduce carrageenan-induced paw edema and inflammatory nociception.	Carrageenan	20-31	programmed cell death 1	Mus musculus	5-8
29149031-7	2017	PD1 can significantly inhibit carrageenan-induced leukocyte infiltration, as well as the protein expression of inflammatory mediators (iNOS, interleukin-1beta, and myeloperoxidase) in inflammatory tissue.	Carrageenan	30-41	programmed cell death 1	Mus musculus	0-3
28681455-7	2017	In the murine GL261 malignant glioma model, there was a similar upregulation of PD-1 on brain-infiltrating lymphocytes.	gl261	14-19	programmed cell death 1	Mus musculus	80-84
29123953-5	2017	Expression of PD-1 and PD-L1 on NB and effector cells was analyzed by RT-PCR and flow cytometry in the presence of ch14.18/CHO and/or IL-2.	CAV protocol	123-126	programmed cell death 1	Mus musculus	14-18
29123953-6	2017	The effect of PD-1 blockade on ch14.18/CHO-mediated anti-NB immune response was evaluated using anti-PD-1 Ab both in vitro (Nivolumab) and in a syngeneic PD-L1+/GD2+ NB mouse model (anti-mouse PD-1).	CAV protocol	39-42	programmed cell death 1	Mus musculus	14-18
29123953-11	2017	In conclusion, ch14.18/CHO-mediated effects upregulate the inhibitory immune checkpoint PD-1/PD-L1, and combination of ch14.18/CHO with PD-1 blockade results in synergistic treatment effects in mice representing a new effective treatment strategy against GD2-positive cancers.	CAV protocol	23-26	programmed cell death 1	Mus musculus	88-92
29123953-11	2017	In conclusion, ch14.18/CHO-mediated effects upregulate the inhibitory immune checkpoint PD-1/PD-L1, and combination of ch14.18/CHO with PD-1 blockade results in synergistic treatment effects in mice representing a new effective treatment strategy against GD2-positive cancers.	CAV protocol	23-26	programmed cell death 1	Mus musculus	136-140
29123953-11	2017	In conclusion, ch14.18/CHO-mediated effects upregulate the inhibitory immune checkpoint PD-1/PD-L1, and combination of ch14.18/CHO with PD-1 blockade results in synergistic treatment effects in mice representing a new effective treatment strategy against GD2-positive cancers.	CAV protocol	127-130	programmed cell death 1	Mus musculus	88-92
29123953-11	2017	In conclusion, ch14.18/CHO-mediated effects upregulate the inhibitory immune checkpoint PD-1/PD-L1, and combination of ch14.18/CHO with PD-1 blockade results in synergistic treatment effects in mice representing a new effective treatment strategy against GD2-positive cancers.	CAV protocol	127-130	programmed cell death 1	Mus musculus	136-140
28404894-12	2017	Furthermore, we observed that both PD-1 or CTLA-4 blockade augmented antitumor effects of ValloVax.	vallovax	90-98	programmed cell death 1	Mus musculus	35-39
28054961-1	2017	Previously, the authors found that 4-hydroxy-2-(4-hydroxyphenethyl) isoindoline-1,3-dione (PD1) (a phthalimide analogue) bound to and activated peroxisome proliferator-activated receptor-gamma (PPAR-gamma).	4-hydroxy-2-(4-hydroxyphenethyl) isoindoline-1,3-dione	35-89	programmed cell death 1	Mus musculus	91-94
28345001-7	2017	The rapamycin plus prednisolone treatment also significantly reduced frequencies of IgD-IgG+ class-switched/FAS+CL7+ germinal center B cells, and of activated CD4+ T cells expressing PD1 and GL7, in spleen.	Sirolimus	4-13	programmed cell death 1	Mus musculus	183-186
28345001-7	2017	The rapamycin plus prednisolone treatment also significantly reduced frequencies of IgD-IgG+ class-switched/FAS+CL7+ germinal center B cells, and of activated CD4+ T cells expressing PD1 and GL7, in spleen.	Prednisolone	19-31	programmed cell death 1	Mus musculus	183-186
28054961-1	2017	Previously, the authors found that 4-hydroxy-2-(4-hydroxyphenethyl) isoindoline-1,3-dione (PD1) (a phthalimide analogue) bound to and activated peroxisome proliferator-activated receptor-gamma (PPAR-gamma).	phthalimide	99-110	programmed cell death 1	Mus musculus	91-94
28054961-3	2017	In lipopolysaccharide (LPS)-stimulated murine RAW264.7 macrophages, PD1 suppressed the inductions of pro-inflammatory factors, including inducible nitric oxide synthase (iNOS), nitric oxide (NO), cyclooxygenase 2 (COX-2), tumor necrosis factor alpha (TNF-alpha), interleukin-1beta (IL-1beta), and interleukin-6 (IL-6).	Nitric Oxide	147-159	programmed cell death 1	Mus musculus	68-71
28054961-7	2017	In a subsequent in vivo animal experiment conducted using a carrageenan-induced acute inflammatory rat paw edema model, intraperitoneal injection of PD1 significantly reduced paw swelling.	Carrageenan	60-71	programmed cell death 1	Mus musculus	149-152
27895178-7	2017	These data implicate a critical role for CR-C in governing PD-1 expression, and a subsequent role in guiding CD8 T cell differentiation.	cr-c	41-45	programmed cell death 1	Mus musculus	59-63
27599066-4	2016	The embedded immunotherapeutic nanocapsule loaded with anti-PD1 antibody (aPD1) is assembled from hyaluronic acid modified with 1-methyl-dl-tryptophan (1-MT), an inhibitor of IDO.	Hyaluronic Acid	98-113	programmed cell death 1	Mus musculus	60-63
28066430-7	2016	After 15 days of treatment, ATV increased the percentage of glucocorticoid-induced tumor necrosis factor receptor-related protein (GITR+) and programmed cell death protein 1 (PD-1+) Tregs in the lung, without enhancing their suppressive activity, but also increased the percentage of conventional T cells expressing GITR+, PD1+, and OX-40 (tumor necrosis factor receptor superfamily member 4).	Atorvastatin	28-31	programmed cell death 1	Mus musculus	142-173
27599066-4	2016	The embedded immunotherapeutic nanocapsule loaded with anti-PD1 antibody (aPD1) is assembled from hyaluronic acid modified with 1-methyl-dl-tryptophan (1-MT), an inhibitor of IDO.	1-methyltryptophan	128-150	programmed cell death 1	Mus musculus	60-63
26859684-4	2016	Using a panel of PD-L1-expressing human and mouse breast and prostate cancer cell lines, we found that incubation of breast and prostate cancer cells in the presence of purified recombinant PD-1 resulted in resistance to doxorubicin and docetaxel as determined using clonogenic survival assays.	Doxorubicin	221-232	programmed cell death 1	Mus musculus	190-194
26859684-4	2016	Using a panel of PD-L1-expressing human and mouse breast and prostate cancer cell lines, we found that incubation of breast and prostate cancer cells in the presence of purified recombinant PD-1 resulted in resistance to doxorubicin and docetaxel as determined using clonogenic survival assays.	Docetaxel	237-246	programmed cell death 1	Mus musculus	190-194
26859684-6	2016	Moreover, inhibition of the PD-1/PD-L1 axis using anti-PD-1 antibody enhanced doxorubicin chemotherapy to inhibit metastasis in a syngeneic mammary orthotopic mouse model of metastatic breast cancer.	Doxorubicin	78-89	programmed cell death 1	Mus musculus	28-32
26859684-6	2016	Moreover, inhibition of the PD-1/PD-L1 axis using anti-PD-1 antibody enhanced doxorubicin chemotherapy to inhibit metastasis in a syngeneic mammary orthotopic mouse model of metastatic breast cancer.	Doxorubicin	78-89	programmed cell death 1	Mus musculus	55-59
27141356-7	2016	Interestingly, the administration of Gem and rlipo-E7m/CpG reduced the quantity of programmed cell death protein 1 (PD-1)-expressing antigen-specific cytotoxic T lymphocytes (CTLs) in the regressing tumors.	gemcitabine	37-40	programmed cell death 1	Mus musculus	83-114
26573793-5	2015	In particular, tumor-bearing mice treated with a combination of paclitaxel and a PD-L1/PD-1 signal blockade survived longer than mice treated with paclitaxel alone.	Paclitaxel	147-157	programmed cell death 1	Mus musculus	87-91
26529122-0	2015	The Combination of Anti-CTLA-4 and PD1-/- Mice Unmasks the Potential of Isoniazid and Nevirapine To Cause Liver Injury.	Isoniazid	72-81	programmed cell death 1	Mus musculus	35-38
26529122-0	2015	The Combination of Anti-CTLA-4 and PD1-/- Mice Unmasks the Potential of Isoniazid and Nevirapine To Cause Liver Injury.	Nevirapine	86-96	programmed cell death 1	Mus musculus	35-38
27141356-7	2016	Interestingly, the administration of Gem and rlipo-E7m/CpG reduced the quantity of programmed cell death protein 1 (PD-1)-expressing antigen-specific cytotoxic T lymphocytes (CTLs) in the regressing tumors.	gemcitabine	37-40	programmed cell death 1	Mus musculus	116-120
26307602-8	2015	A (64)Cu labeled anti-mouse antibody (IgG) PD-1 immuno positron emission tomography (PET) tracer was developed to detect PD-1 expressing murine TILs.	Copper	6-8	programmed cell death 1	Mus musculus	43-47
26307602-8	2015	A (64)Cu labeled anti-mouse antibody (IgG) PD-1 immuno positron emission tomography (PET) tracer was developed to detect PD-1 expressing murine TILs.	Copper	6-8	programmed cell death 1	Mus musculus	121-125
26162855-9	2015	In addition, long-term use of indomethacin activates TRIF/NF-kappaB and JAK/STAT3 pathways, and indomethacin promotes the expression of PD-1 and PD-L2 via TRIF/NF-kappaB pathway and JAK/STAT3 pathway respectively in gammadelta T cells.	Indomethacin	96-108	programmed cell death 1	Mus musculus	136-140
26162855-10	2015	Given these findings, we drew a conclusion that long-term use of indomethacin leads to poor prognoses through promoting the expression of PD-1 and PD-L2 via TRIF/NF-kappaB pathway and JAK/STAT3 pathway to inhibit TNF-alpha and IFN-gamma in HCC.	Indomethacin	65-77	programmed cell death 1	Mus musculus	138-142
26162855-0	2015	Long-term use of indomethacin leads to poor prognoses through promoting the expression of PD-1 and PD-L2 via TRIF/NF-kappaB pathway and JAK/STAT3 pathway to inhibit TNF-alpha and IFN-gamma in hepatocellular carcinoma.	Indomethacin	17-29	programmed cell death 1	Mus musculus	90-94
26162855-7	2015	Furthermore, long-term use of indomethacin increased the expression of PD-1 and PD-L2 in programmed death-1 pathway.	Indomethacin	30-42	programmed cell death 1	Mus musculus	71-75
26154582-0	2015	The Role of CD8 T Cells in Amodiaquine-Induced Liver Injury in PD1-/- Mice Cotreated with Anti-CTLA-4.	Amodiaquine	27-38	programmed cell death 1	Mus musculus	63-66
26162855-8	2015	Blockade of PD-1 and PD-L2 reversed the reduced production of TNF-alpha and IFN-gamma induced by indomethacin in gammadelta T cells.	Indomethacin	97-109	programmed cell death 1	Mus musculus	12-16
26154582-4	2015	Recently our laboratory reported a model of amodiaquine (AQ)-induced IDILI using PD1-/- mice and an anti-CTLA4 antibody.	Amodiaquine	44-55	programmed cell death 1	Mus musculus	81-84
26154582-4	2015	Recently our laboratory reported a model of amodiaquine (AQ)-induced IDILI using PD1-/- mice and an anti-CTLA4 antibody.	Amodiaquine	57-59	programmed cell death 1	Mus musculus	81-84
26408258-2	2015	In a preventative CT26 mouse tumor model, both doxorubicin and Doxil synergized with anti-PD-1 and CTLA-4 mAbs.	Doxorubicin	47-58	programmed cell death 1	Mus musculus	90-94
26266810-7	2015	GL261GSCs were intracranially implanted into mice, and the mice were stratified into 3 treatment groups: 1) control, 2) NK cells treatment, and 3) PD-1 inhibited NK cells treatment group.	gl261gscs	0-9	programmed cell death 1	Mus musculus	147-151
27057439-4	2016	In two cancer models, B16-F10 melanoma and 4T1 metastatic breast cancer, the alginate hydrogel delivery system significantly improves the antitumor activities of celecoxib (CXB), PD-1 mAb, or both combined.	Alginates	77-85	programmed cell death 1	Mus musculus	179-183
27057439-9	2016	This alginate-hydrogel-mediated, combinatorial therapy of celecoxib and PD-1 mAb provides a potential valuable regimen for treating human cancer.	Alginates	5-13	programmed cell death 1	Mus musculus	72-76
27057446-8	2016	Anti-PD-1 associated toxicities were alleviated when PD-1 blockade was combined with the therapeutic HSP90 inhibitor, ganetespib, which impaired immune responses toward the xenogeneic PD-1 mAb.	STA 9090	118-128	programmed cell death 1	Mus musculus	5-9
27057446-8	2016	Anti-PD-1 associated toxicities were alleviated when PD-1 blockade was combined with the therapeutic HSP90 inhibitor, ganetespib, which impaired immune responses toward the xenogeneic PD-1 mAb.	STA 9090	118-128	programmed cell death 1	Mus musculus	53-57
27057446-8	2016	Anti-PD-1 associated toxicities were alleviated when PD-1 blockade was combined with the therapeutic HSP90 inhibitor, ganetespib, which impaired immune responses toward the xenogeneic PD-1 mAb.	STA 9090	118-128	programmed cell death 1	Mus musculus	53-57
26408258-2	2015	In a preventative CT26 mouse tumor model, both doxorubicin and Doxil synergized with anti-PD-1 and CTLA-4 mAbs.	Doxorubicin	63-68	programmed cell death 1	Mus musculus	90-94
25973021-6	2015	The expression of MHC, cluster of differentiation 86 (CD86), PD-1 and PD-L1 in spleen DCs were increased at early stage after zymosan injection.	Zymosan	126-133	programmed cell death 1	Mus musculus	61-65
26048148-6	2015	Three-fold increases in the percentage of IL-17A(+) GDL T cells were observed in skin cell suspensions derived from IMQ-treated PD-1KO mice (versus WT controls), suggesting that the lack of PD-1 has a functional effect not only on alphabeta T cells, but also on GDL T cells, and that PD-1 may play a regulatory role in PsD.	Imiquimod	116-119	programmed cell death 1	Mus musculus	128-132
25624454-2	2015	We found that PD-1(-/-) mice, as well as wild-type mice treated with a PD-1 blocking Ab, exhibited significantly increased survival against lethal Streptococcus pneumoniae infection following either priming with low-dose pneumococcal respiratory infection or S. pneumoniae-capsular polysaccharide immunization.	Polysaccharides	282-296	programmed cell death 1	Mus musculus	14-18
25624454-2	2015	We found that PD-1(-/-) mice, as well as wild-type mice treated with a PD-1 blocking Ab, exhibited significantly increased survival against lethal Streptococcus pneumoniae infection following either priming with low-dose pneumococcal respiratory infection or S. pneumoniae-capsular polysaccharide immunization.	Polysaccharides	282-296	programmed cell death 1	Mus musculus	71-75
25877890-6	2015	When combined with PD-1 (programmed death 1) blockade, STINGVAX induced regression of palpable, poorly immunogenic tumors that did not respond to PD-1 blockade alone.	stingvax	55-63	programmed cell death 1	Mus musculus	19-23
25877890-6	2015	When combined with PD-1 (programmed death 1) blockade, STINGVAX induced regression of palpable, poorly immunogenic tumors that did not respond to PD-1 blockade alone.	stingvax	55-63	programmed cell death 1	Mus musculus	25-43
25877890-6	2015	When combined with PD-1 (programmed death 1) blockade, STINGVAX induced regression of palpable, poorly immunogenic tumors that did not respond to PD-1 blockade alone.	stingvax	55-63	programmed cell death 1	Mus musculus	146-150
24502656-11	2014	More importantly, combined treatment of anti-PD-1/GITR mAb and chemotherapeutic drugs (cisplatin or paclitaxel) further increased the antitumor efficacy with 80% of mice obtaining tumor-free long-term survival in murine ID8 ovarian cancer and 4 T1 breast cancer models.	Cisplatin	87-96	programmed cell death 1	Mus musculus	45-49
25415283-7	2015	In addition, combination therapy with vaccine and PD-1 antibody blockade improved murine survival compared with PD-1 antibody monotherapy or GVAX therapy alone.	gvax	141-145	programmed cell death 1	Mus musculus	50-54
25082815-6	2014	We found that PD1 and CTLA4 antagonists showed limited efficacy as single agents to restrain PDAC growth, but that combining these agents with CSF1R blockade potently elicited tumor regressions, even in larger established tumors.	pdac	93-97	programmed cell death 1	Mus musculus	14-17
24886298-2	2014	METHODS: In this study, the expression of PD-1 and its ligands, PD-L1 and PD-L2, in uterine tissues from aged WT mice in a 129svEv-Brd background was analyzed by immunohistochemistry and the uterine morphology between WT and PD-1-/- mice was compared by hematoxylin and eosin staining.	Hematoxylin	254-265	programmed cell death 1	Mus musculus	42-46
24886298-2	2014	METHODS: In this study, the expression of PD-1 and its ligands, PD-L1 and PD-L2, in uterine tissues from aged WT mice in a 129svEv-Brd background was analyzed by immunohistochemistry and the uterine morphology between WT and PD-1-/- mice was compared by hematoxylin and eosin staining.	Eosine Yellowish-(YS)	270-275	programmed cell death 1	Mus musculus	42-46
24462405-9	2014	When these CD8(+) cells were re-stimulated in vitro with LPG, simulating a second exposure to parasite antigens, PD-1 expression increased significantly more, in a dose dependent fashion.	lipophosphonoglycan	57-60	programmed cell death 1	Mus musculus	113-117
24502656-11	2014	More importantly, combined treatment of anti-PD-1/GITR mAb and chemotherapeutic drugs (cisplatin or paclitaxel) further increased the antitumor efficacy with 80% of mice obtaining tumor-free long-term survival in murine ID8 ovarian cancer and 4 T1 breast cancer models.	Paclitaxel	100-110	programmed cell death 1	Mus musculus	45-49
23686636-3	2013	Here we report that perisurgical treatment of neuroprotectin D1/protectin D1 (NPD1/PD1), derived from docosahexaenoic acid, prevents nerve injury-induced mechanical allodynia and ongoing pain in mice.	Docosahexaenoic Acids	102-122	programmed cell death 1	Mus musculus	79-82
23098512-2	2012	Here we evaluated the anti-tumor efficacy of AAV-mediated delivery of the extracellular domain of murine PD-1 (sPD-1) to a tumor site.	CHEMBL2031461	45-48	programmed cell death 1	Mus musculus	105-109
23303666-0	2013	Naturally occurring PD-1+ memory phenotype CD8 T cells belong to nonconventional CD8 T cells and are cyclophosphamide-sensitive regulatory T cells.	Cyclophosphamide	101-117	programmed cell death 1	Mus musculus	20-24
23303666-8	2013	PD-1(+) MP CD8 T cells showed the fastest cell cycling among various T cell subsets in naive mice, which was consistent with the highest sensitivity to cyclophosphamide (CP) treatment.	Cyclophosphamide	152-168	programmed cell death 1	Mus musculus	0-4
23853599-6	2013	Surprisingly, coadministration of an agonistic anti-CD40 antibody (alphaCD40) inhibited PD-1 induction and restored T cell effector function, thereby inhibiting viral gene expression and causing a necroinflammatory liver disease.	alphacd40	67-76	programmed cell death 1	Mus musculus	88-92
23039230-2	2012	Our previous studies demonstrated that oestrogen (17beta-oestradiol; E(2) ) protection against experimental autoimmune encephalomyelitis (EAE) is mediated mainly through oestrogen receptor-alpha (ERalpha) and the membrane receptor G-protein-coupled receptor 30 (GPR30) and is abrogated in the absence of B cells and the co-inhibitory receptor, Programmed Death-1 (PD-1).	Estradiol	50-67	programmed cell death 1	Mus musculus	364-368
23908592-6	2013	In addition, silica-mediated inflammation generated an immunosuppressive microenvironment in which we observed increased expression of programmed cell death protein 1 (PD-1), transforming growth factor-beta1, monocyte chemotactic protein 1 (MCP-1), lymphocyte-activation gene 3 (LAG3), and forkhead box P3 (FOXP3), as well as the presence of regulatory T cells.	Silicon Dioxide	13-19	programmed cell death 1	Mus musculus	135-166
21116786-4	2010	The incidence of autoimmune diabetes induced by multiple low dose of streptozotocin (STZ) was reduced in PD-1 Tg mice.	Streptozocin	69-83	programmed cell death 1	Mus musculus	105-109
21906434-2	2011	We investigated the associative role of programmed death-1 (PD-1) gene in the pathogenesis of KD by injecting bacilli Calmette Guerin (BCG) to PD-1 gene knockout (PD-1KO) mice.	bacilli calmette guerin	110-133	programmed cell death 1	Mus musculus	60-64
21116786-4	2010	The incidence of autoimmune diabetes induced by multiple low dose of streptozotocin (STZ) was reduced in PD-1 Tg mice.	Streptozocin	85-88	programmed cell death 1	Mus musculus	105-109
21116786-5	2010	Although the expression of CTLA-4, PD-1 and FoxP3, which are inhibitory molecules of activated T cells, is reduced only on STZ injected wild type (WT) mice, CD4, CD8 and regulatory T cell populations were not changed in all experimental groups.	Streptozocin	123-126	programmed cell death 1	Mus musculus	35-39
21116786-7	2010	Interestingly, macrophages were observed in splenocytes of STZ injected PD-1 Tg at somewhat lower level than macrophage in diabetic wild type mice.	Streptozocin	59-62	programmed cell death 1	Mus musculus	72-76
19811462-5	2009	Cytotoxic T lymphocyte antigen-4 (CTLA-4) and Programmed cell death 1 (PD-1) are some of known Treg-associated molecules; however, their role in Treg-mediated fetal protection in murine model has not been investigated.	treg	95-99	programmed cell death 1	Mus musculus	71-75
20160101-3	2010	Here, we show that the combination of CTLA-4 and PD-1 blockade is more than twice as effective as either alone in promoting the rejection of B16 melanomas in conjunction with Fvax.	fvax	175-179	programmed cell death 1	Mus musculus	49-53
20186864-0	2010	Preventive role of PD-1 on MPTP-induced dopamine depletion in mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	27-31	programmed cell death 1	Mus musculus	19-23
20186864-0	2010	Preventive role of PD-1 on MPTP-induced dopamine depletion in mice.	Dopamine	40-48	programmed cell death 1	Mus musculus	19-23
20186864-3	2010	This study was designed to investigate the effect of PD-1 extract in the Parkinson"s model of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) lesioned mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	94-138	programmed cell death 1	Mus musculus	53-57
20186864-3	2010	This study was designed to investigate the effect of PD-1 extract in the Parkinson"s model of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) lesioned mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	140-144	programmed cell death 1	Mus musculus	53-57
20186864-6	2010	Oral administration of PD-1 extract (50 and 100 mg kg(-1)) attenuated the MPTP-induced depletion of TH proteins in the striatum and SNpc and prevented the apoptotic effects.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	74-78	programmed cell death 1	Mus musculus	23-27
20186864-7	2010	These results indicate that PD-1 extract is able to protect dopaminergic neurons from MPTP-induced neuronal death, with important implications for the treatment of PD.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	86-90	programmed cell death 1	Mus musculus	28-32
19642196-8	2010	Therefore, down-modulation of PD-1 in Treg cells may abrogate Treg-mediated immune suppression, permitting the activation of myelin-reactive T cells and induction of EAE.	treg	38-42	programmed cell death 1	Mus musculus	30-34
19811462-10	2009	RESULTS: Blocking PD-1 abrogated the protective effect of Treg, resulting in a higher median abortion rate in comparison with the Treg/isotype-treated control while CTLA-4 blockage did not interfere with the protective effect of Treg.	treg	58-62	programmed cell death 1	Mus musculus	18-22
15663901-6	2005	RESULTS: When mifepristone was given on Pd1, developing and fully developed pinopodes were observed, but the expression was markedly reduced compared to the control group.	Mifepristone	14-26	programmed cell death 1	Mus musculus	40-43
19302141-2	2009	We here demonstrate that treatment with 17beta-oestradiol (E(2)) in C57BL/6 mice boosted the expression of programmed death 1 (PD-1), a negative regulator of immune responses, in the CD4(+) FoxP3(+) regulatory T (Treg) cell compartment in a dose-dependent manner that correlated with the efficiency of EAE protection.	Estradiol	40-57	programmed cell death 1	Mus musculus	107-125
19302141-2	2009	We here demonstrate that treatment with 17beta-oestradiol (E(2)) in C57BL/6 mice boosted the expression of programmed death 1 (PD-1), a negative regulator of immune responses, in the CD4(+) FoxP3(+) regulatory T (Treg) cell compartment in a dose-dependent manner that correlated with the efficiency of EAE protection.	Estradiol	40-57	programmed cell death 1	Mus musculus	127-131
19302141-7	2009	Taken together, our results suggest that E(2)-induced protection against EAE is mediated by upregulation of PD-1 expression within the Treg-cell compartment.	Estradiol	41-45	programmed cell death 1	Mus musculus	108-112
18479731-12	2008	Because the anti-PD-1.6.4 antibody works on paraffin sections, it represents a useful tool to differentiate SLL/CLL from other small B-cell lymphomas.	Paraffin	44-52	programmed cell death 1	Mus musculus	17-21
17552908-1	2007	We studied the interaction of the artificial 12-aa proline-rich peptide PD1 with the SH3 domain of the hematopoietic cell kinase Hck and the peptide"s potency in competitively displacing HIV-1 Nef from the Hck SH3 domain.	Proline	51-58	programmed cell death 1	Mus musculus	72-75
16900095-0	2006	A protective role for programmed death 1 in progression of murine adriamycin nephropathy.	Doxorubicin	66-76	programmed cell death 1	Mus musculus	22-40
19710450-7	2009	PD-1 blockade also selectively rescued PPS-3-specific IgG3 responses in CD21/35(-/-) mice.	Pentosan Sulfuric Polyester	39-42	programmed cell death 1	Mus musculus	0-4
19781375-6	2009	RESULTS: The expression levels of PD-1, PD-L1, PD-L2 mRNA were higher in EAH compared with normal controls (P &lt; 0.05), the PD-L2/PD-1 ratio was relatively lower in EAH (EAH -0.08 +/- 0.35, normal controls 0.52 +/- 0.07, P = 0.009).	eah	73-76	programmed cell death 1	Mus musculus	34-38
19781375-10	2009	CONCLUSIONS: The expression of PD-1/PD-L1, L2 is upregulated in EAH and regulated by IFN-gamma and IL-4.	eah	64-67	programmed cell death 1	Mus musculus	31-35
19447898-11	2009	Hence, PD-1 may be a conduit for reversing AHR by Tregs and a plausible target for treating asthma.	tregs	50-55	programmed cell death 1	Mus musculus	7-11
15663901-10	2005	CONCLUSION: These findings suggest that administration of a single dose of RU486 subcutaneously on Pd1, Pd2, Pd3, and Pd4 might play a role in inhibiting development and maturation of endometrium, hence affecting embryo implantation in mice.	Mifepristone	75-80	programmed cell death 1	Mus musculus	99-102
14662900-8	2003	Prolonged islet allograft survival achieved by blockade of the MCP-1/CCR2 pathway plus rapamycin therapy was accompanied by a mononuclear cell infiltrate expressing the inhibitory receptor, programmed death-1 (PD-1), and its ligand (PD-L1, B7-H1), and prolongation of islet allograft survival was abrogated by anti-PD-L1 mAb therapy.	Sirolimus	87-96	programmed cell death 1	Mus musculus	190-208
14662900-8	2003	Prolonged islet allograft survival achieved by blockade of the MCP-1/CCR2 pathway plus rapamycin therapy was accompanied by a mononuclear cell infiltrate expressing the inhibitory receptor, programmed death-1 (PD-1), and its ligand (PD-L1, B7-H1), and prolongation of islet allograft survival was abrogated by anti-PD-L1 mAb therapy.	Sirolimus	87-96	programmed cell death 1	Mus musculus	210-214
12538684-2	2003	PD-1 contains an immunoreceptor tyrosine-based inhibitory motif and mice deficient in PD-1 develop autoimmune disorders suggesting a defect in peripheral tolerance.	Tyrosine	32-40	programmed cell death 1	Mus musculus	0-4
14568931-9	2003	Increased annexin V(+) cells among the DP population argued for augmented negative selection in PD-1(-/-) mice.	dp	39-41	programmed cell death 1	Mus musculus	96-100
12538684-2	2003	PD-1 contains an immunoreceptor tyrosine-based inhibitory motif and mice deficient in PD-1 develop autoimmune disorders suggesting a defect in peripheral tolerance.	Tyrosine	32-40	programmed cell death 1	Mus musculus	86-90
11857337-1	2002	Programmed death-1 (PD-1) is an immunoreceptor tyrosine-based inhibitory motif (ITIM)-containing receptor expressed upon T cell activation.	Tyrosine	47-55	programmed cell death 1	Mus musculus	0-18
11857337-1	2002	Programmed death-1 (PD-1) is an immunoreceptor tyrosine-based inhibitory motif (ITIM)-containing receptor expressed upon T cell activation.	Tyrosine	47-55	programmed cell death 1	Mus musculus	20-24
10485649-1	1999	PD-1, a 55 kDa transmembrane protein containing an immunoreceptor tyrosine-based inhibitory motif, is induced in lymphocytes and monocytic cells following activation.	Tyrosine	66-74	programmed cell death 1	Mus musculus	0-4
9796923-1	1998	PD-1, an Ig superfamily member, contains an immunoreceptor tyrosine-based inhibitory motif in the cytoplasmic tail.	Tyrosine	59-67	programmed cell death 1	Mus musculus	0-4