PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
33770574-0	2021	Design, synthesis, and structure-activity relationship of programmed cell death-1/programmed cell death-ligand 1 interaction inhibitors bearing a benzo[d]isothiazole scaffold.	benzisothiazole	146-165	programmed cell death 1	Sus scrofa	58-112
21268005-7	2011	When PD-1(+) gammadelta T cells were challenged by PD-L1(+) tumors pretreated with zoledronate (Zol), which induced gammadelta TCR-mediated signaling, the resulting reduction in cytokine production was only slight to moderate compared to the reduction seen when PD-1(+) gammadelta T cells were challenged by PD-L1(-) tumors.	Zoledronic Acid	83-94	programmed cell death 1	Sus scrofa	5-9
21268005-7	2011	When PD-1(+) gammadelta T cells were challenged by PD-L1(+) tumors pretreated with zoledronate (Zol), which induced gammadelta TCR-mediated signaling, the resulting reduction in cytokine production was only slight to moderate compared to the reduction seen when PD-1(+) gammadelta T cells were challenged by PD-L1(-) tumors.	Zoledronic Acid	83-94	programmed cell death 1	Sus scrofa	262-266
21268005-7	2011	When PD-1(+) gammadelta T cells were challenged by PD-L1(+) tumors pretreated with zoledronate (Zol), which induced gammadelta TCR-mediated signaling, the resulting reduction in cytokine production was only slight to moderate compared to the reduction seen when PD-1(+) gammadelta T cells were challenged by PD-L1(-) tumors.	Zoledronic Acid	96-99	programmed cell death 1	Sus scrofa	5-9
21268005-7	2011	When PD-1(+) gammadelta T cells were challenged by PD-L1(+) tumors pretreated with zoledronate (Zol), which induced gammadelta TCR-mediated signaling, the resulting reduction in cytokine production was only slight to moderate compared to the reduction seen when PD-1(+) gammadelta T cells were challenged by PD-L1(-) tumors.	Zoledronic Acid	96-99	programmed cell death 1	Sus scrofa	262-266
21268005-8	2011	In addition, cytotoxic activity of PD-1(+) gammadelta T cells against Zol-treated PD-L1(+) tumors was comparable to that against Zol-treated PD-L1(-) tumors.	Zoledronic Acid	70-73	programmed cell death 1	Sus scrofa	35-39
34839997-0	2022	Discovery of quinazoline derivatives as novel small-molecule inhibitors targeting the programmed cell death-1/programmed cell death-ligand 1 (PD-1/PD-L1) interaction.	Quinazolines	13-24	programmed cell death 1	Sus scrofa	86-140
34937742-6	2021	RESULTS: We find that Vdelta2 T cells expanded by IPP plus resiquimod showed significantly increased cytotoxicity to tumor cells with lower programmed cell death protein 1 (PD-1) expression than Vdelta2 T cells expanded by IPP or ZOL.	isopentenyl pyrophosphate	50-53	programmed cell death 1	Sus scrofa	140-171
34592487-6	2021	Flow cytometry were used to analyze the effects of Curcumin on the expression of programmed cell death protein 1 (PD-1) and T-cell immunoglobulin and mucin-domain3 (TIM-3) on CD4, CD8 and Treg.	Curcumin	51-59	programmed cell death 1	Sus scrofa	81-112
34321275-11	2021	Furthermore, the combination of decitabine with programmed cell death protein 1 (PD-1) inhibitor reversed T cell exhaustion and improved T cell function in mouse models, which elicited potent antitumor activity in MYC-overexpressing TNBC.	Decitabine	32-42	programmed cell death 1	Sus scrofa	48-79
35387972-3	2022	The controlled TAM depletion creates a favorable milieu for facilitating local and systemic delivery of anti-programmed cell death protein 1 (aPD-1) antibody-conjugated platelets to inhibit post-surgery tumor recurrence.	tam	15-18	programmed cell death 1	Sus scrofa	109-140
35365585-1	2022	BACKGROUND: Targeting the PD-1/PD-L1/L2 (programmed cell death protein 1/programmed cell death ligand 1/ligand 2) pathway combined with other immunosuppressive signalings, such as CD73/A2aR (A2a adenosine receptor) adenosine signaling, has emerged as a promising strategy for cancer treatment.	Adenosine	215-224	programmed cell death 1	Sus scrofa	41-112
31731885-5	2020	However, metformin over 24 weeks led to decreases compared to OBS in single PD1+ (percent decrease: -9.6% vs 7.5%, p=0.015), in dual PD1+TIGIT+ (-15.0% vs 10.4%, p=0.002) and in triple PD1+TIGIT+TIM3+ (-24.0% vs 8.1%, p=0.041) CD4 T-cells.	Metformin	9-18	programmed cell death 1	Sus scrofa	76-79
32902555-0	2020	Microneedles loaded with anti-PD-1-cisplatin nanoparticles for synergistic cancer immuno-chemotherapy.	Cisplatin	35-44	programmed cell death 1	Sus scrofa	30-34
32913444-2	2020	In addition, recent studies have revealed that tumor microsatellite instability (MSI) status and tumor mutation burden (TMB) contribute significantly to the therapeutic response to anti-PD-1 monoclonal antibody (mAb), which led to an accelerated approval to pembrolizumab for the treatment of MSI-high or mismatch-repair-deficient solid tumors after conventional chemotherapies in 2017 and for the treatment of TMB-high solid tumors in 2020 by the United States Food and Drug Administration (FDA).	1,2,4,5-tetramethoxybenzene	120-123	programmed cell death 1	Sus scrofa	186-190
32066859-8	2020	CPS >= 1 SBAs showed higher TIL and PD-1+ immune cell density, more frequently medullary histotype, as well as a better outcome in comparison with CPS < 1 cases.	cps	0-3	programmed cell death 1	Sus scrofa	36-40
31731885-5	2020	However, metformin over 24 weeks led to decreases compared to OBS in single PD1+ (percent decrease: -9.6% vs 7.5%, p=0.015), in dual PD1+TIGIT+ (-15.0% vs 10.4%, p=0.002) and in triple PD1+TIGIT+TIM3+ (-24.0% vs 8.1%, p=0.041) CD4 T-cells.	Metformin	9-18	programmed cell death 1	Sus scrofa	133-136
31731885-5	2020	However, metformin over 24 weeks led to decreases compared to OBS in single PD1+ (percent decrease: -9.6% vs 7.5%, p=0.015), in dual PD1+TIGIT+ (-15.0% vs 10.4%, p=0.002) and in triple PD1+TIGIT+TIM3+ (-24.0% vs 8.1%, p=0.041) CD4 T-cells.	Metformin	9-18	programmed cell death 1	Sus scrofa	133-136
31731885-7	2020	CONCLUSIONS: Metformin decreases the frequency of PD1+, PD1+TIGIT+ and PD1+TIGIT+TIM3+ expressing CD4 T-cells.	Metformin	13-22	programmed cell death 1	Sus scrofa	50-53
31731885-7	2020	CONCLUSIONS: Metformin decreases the frequency of PD1+, PD1+TIGIT+ and PD1+TIGIT+TIM3+ expressing CD4 T-cells.	Metformin	13-22	programmed cell death 1	Sus scrofa	56-59
31731885-7	2020	CONCLUSIONS: Metformin decreases the frequency of PD1+, PD1+TIGIT+ and PD1+TIGIT+TIM3+ expressing CD4 T-cells.	Metformin	13-22	programmed cell death 1	Sus scrofa	56-59
31770816-8	2020	CONCLUSIONS: Our study suggests that Pdcd1 methylation is correlated with PD-1 expression on CD8+ T cells and correlated with HBsAg and alanine aminotransferase (ALT).	Alanine	136-143	programmed cell death 1	Sus scrofa	37-42
32184441-3	2020	PD-1 has one immunoreceptor tyrosine-based inhibitory motif (ITIM) at Y223 and one immunoreceptor tyrosine-based switch motif (ITSM) at Y248.	Tyrosine	28-36	programmed cell death 1	Sus scrofa	0-4
32184441-3	2020	PD-1 has one immunoreceptor tyrosine-based inhibitory motif (ITIM) at Y223 and one immunoreceptor tyrosine-based switch motif (ITSM) at Y248.	Tyrosine	98-106	programmed cell death 1	Sus scrofa	0-4
32184441-4	2020	Only ITSM-Y248 is indispensable for PD-1-mediated inhibitory function but how SHP-2 enzymatic activation is mechanistically regulated by one PD-1 phosphotyrosine remains a puzzle.	itsm-y248	5-14	programmed cell death 1	Sus scrofa	36-40
32184441-8	2020	Our results unravel a mechanism of PD-1: SHP-2 interaction that depends only on ITSM-Y248 and explain how a single docking site within the PD-1 cytoplasmic tail can activate SHP-2 and PD-1-mediated inhibitory function.	y248	85-89	programmed cell death 1	Sus scrofa	35-39
32184441-8	2020	Our results unravel a mechanism of PD-1: SHP-2 interaction that depends only on ITSM-Y248 and explain how a single docking site within the PD-1 cytoplasmic tail can activate SHP-2 and PD-1-mediated inhibitory function.	y248	85-89	programmed cell death 1	Sus scrofa	139-143
32184441-8	2020	Our results unravel a mechanism of PD-1: SHP-2 interaction that depends only on ITSM-Y248 and explain how a single docking site within the PD-1 cytoplasmic tail can activate SHP-2 and PD-1-mediated inhibitory function.	y248	85-89	programmed cell death 1	Sus scrofa	139-143
31978106-2	2020	The inhibitor of apoptosis protein antagonist Debio 1143 (D1143) enhances tumor cell death and synergizes with anti-PD-1 agents to promote tumor immunity and displayed HIV latency reversal activity in vitro.	N-benzhydryl-5-(2-(methylamino)propanamido)-3-(3-methylbutanoyl)-6-oxodecahydropyrrolo(1,2-a)(1,5)diazocine-8-carboxamide	46-56	programmed cell death 1	Sus scrofa	116-120
31978106-2	2020	The inhibitor of apoptosis protein antagonist Debio 1143 (D1143) enhances tumor cell death and synergizes with anti-PD-1 agents to promote tumor immunity and displayed HIV latency reversal activity in vitro.	N-benzhydryl-5-(2-(methylamino)propanamido)-3-(3-methylbutanoyl)-6-oxodecahydropyrrolo(1,2-a)(1,5)diazocine-8-carboxamide	58-63	programmed cell death 1	Sus scrofa	116-120
29472716-5	2018	In this study, we show that neural crest-derived MSCs from dental pulp (MSC-DP), but not MSCs from bone marrow, expressed PD-1.	dp	76-78	programmed cell death 1	Sus scrofa	122-126
31587253-5	2020	In this study, we silenced the expression of PD-L1 in DCs and programmed cell death protein 1 (PD-1) in T cells by small interfering RNA (siRNA) -loaded chitosan-dextran sulfate nanoparticles (NPs) and evaluated the DC phenotypic and functional characteristics and T-cell functions following tumor antigen recognition on DCs, ex vivo.	Chitosan	153-161	programmed cell death 1	Sus scrofa	62-93
31587253-5	2020	In this study, we silenced the expression of PD-L1 in DCs and programmed cell death protein 1 (PD-1) in T cells by small interfering RNA (siRNA) -loaded chitosan-dextran sulfate nanoparticles (NPs) and evaluated the DC phenotypic and functional characteristics and T-cell functions following tumor antigen recognition on DCs, ex vivo.	Dextran Sulfate	162-177	programmed cell death 1	Sus scrofa	62-93
33565499-1	2020	Immune checkpoint blockade with programmed cell death protein-1 (PD-1)/programmed cell death ligand-1 (PD-L1) inhibitors has been standard care for metastatic nonsmall cell lung cancer (NSCLC) and after progression using first-line platinum-containing chemotherapy.	Platinum	232-240	programmed cell death 1	Sus scrofa	32-63
30828801-5	2019	In an immunocompetent murine leukaemia model, guadecitabine negatively regulates inhibitory accessory cells in the TME by decreasing PD-1 (also termed PDCD1) expressing T cells and reducing AML-mediated expansion of myeloid-derived suppressor cells.	guadecitabine	46-59	programmed cell death 1	Sus scrofa	133-137
30828801-5	2019	In an immunocompetent murine leukaemia model, guadecitabine negatively regulates inhibitory accessory cells in the TME by decreasing PD-1 (also termed PDCD1) expressing T cells and reducing AML-mediated expansion of myeloid-derived suppressor cells.	guadecitabine	46-59	programmed cell death 1	Sus scrofa	151-156
31455033-8	2019	In contrast, higher counts of stromal PD-1+ cells in the peritoneal lesions have been associated with reduced platinum-sensitivity (p=0.045).	Platinum	110-118	programmed cell death 1	Sus scrofa	38-42
31496815-9	2019	EBV load correlated positively with unfavourable clinical markers of CLL and the expression of PD-1 and PD-L1 on CD4+ and CD8+ cells (rho =0.42-0.75; p&lt;0.001).	(2S)-2-amino-1-[(3aR,6aS)-5-[(5-chloro-1H-indol-3-yl)methyl]hexahydropyrrolo[3,4-c]pyrrol-2(1H)-yl]-3-(1H-indol-3-yl)propan-1-one	0-3	programmed cell death 1	Sus scrofa	95-99
29472716-6	2018	Knocking down PD-1 expression in MSC-DP results in a significantly reduced capacity for cell proliferation and accelerated multipotential differentiation.	dp	37-39	programmed cell death 1	Sus scrofa	14-18
29472716-8	2018	This study indicates that PD-1 is a key surface molecule controlling cell proliferation and multipotential differentiation of MSC-DP.	dp	130-132	programmed cell death 1	Sus scrofa	26-30
29472716-9	2018	Through regulating PD-1/SHP2/ERK signaling, we can significantly improve the quality and quantity of culture-expanded MSC-DP for potential clinical therapies.	dp	122-124	programmed cell death 1	Sus scrofa	19-23
29434366-6	2018	This oncolytic-virus-induced subversion of tumour-associated immunosuppression can potentiate the effectiveness of current immunotherapeutics, including immune checkpoint inhibitors (for example, antibodies against programmed cell death protein 1 (PD1), programmed cell death 1 ligand 1 (PDL1), and cytotoxic T lymphocyte antigen 4 (CTLA4)) and chemotherapeutics that induce immunogenic cell death (for example, doxorubicin and oxaliplatin).	Doxorubicin	412-423	programmed cell death 1	Sus scrofa	248-251
29434366-6	2018	This oncolytic-virus-induced subversion of tumour-associated immunosuppression can potentiate the effectiveness of current immunotherapeutics, including immune checkpoint inhibitors (for example, antibodies against programmed cell death protein 1 (PD1), programmed cell death 1 ligand 1 (PDL1), and cytotoxic T lymphocyte antigen 4 (CTLA4)) and chemotherapeutics that induce immunogenic cell death (for example, doxorubicin and oxaliplatin).	Oxaliplatin	428-439	programmed cell death 1	Sus scrofa	248-251
26330898-4	2015	We observed that stimulation of these neuroimmune cells by METH responded differentially to PD-1/PD-L1 expression.	Methamphetamine	59-63	programmed cell death 1	Sus scrofa	92-96
30068796-0	2018	Macrocyclic Compounds from Ansamycin Antibiotic Class as Inhibitors of PD1-PDL1 Protein-Protein Interaction.	Rifabutin	27-36	programmed cell death 1	Sus scrofa	71-74
30068796-6	2018	In this context, our present study led to the identification of several macrocyclic compounds from the ansamycin antibiotics class to be inhibitors of PD1-PDL1 interaction.	Rifabutin	103-112	programmed cell death 1	Sus scrofa	151-154
28978751-9	2017	ERY974 also induced a robust antitumor efficacy even against tumors with nonimmunogenic features, which are difficult to treat by inhibiting immune checkpoints such as PD-1 (programmed cell death protein-1) and CTLA-4 (cytotoxic T lymphocyte-associated protein-4).	ery974	0-6	programmed cell death 1	Sus scrofa	168-172
28978751-9	2017	ERY974 also induced a robust antitumor efficacy even against tumors with nonimmunogenic features, which are difficult to treat by inhibiting immune checkpoints such as PD-1 (programmed cell death protein-1) and CTLA-4 (cytotoxic T lymphocyte-associated protein-4).	ery974	0-6	programmed cell death 1	Sus scrofa	174-205
28408783-5	2017	We amplified the cDNA encoding the extracellular domains of PD-1 and PD-L1 to construct recombinant expression plasmids and obtain soluble recombinant proteins, which were then labeled with fluorescein isothiocyanate (FITC).	Fluorescein-5-isothiocyanate	190-216	programmed cell death 1	Sus scrofa	60-64
28408783-5	2017	We amplified the cDNA encoding the extracellular domains of PD-1 and PD-L1 to construct recombinant expression plasmids and obtain soluble recombinant proteins, which were then labeled with fluorescein isothiocyanate (FITC).	Fluorescein-5-isothiocyanate	218-222	programmed cell death 1	Sus scrofa	60-64
26330898-6	2015	The response of hBECs to PD-1/PD-L1 induction occurred at 24 hours, while increase of PD-1/PD-L1 levels in neurons and microglia was immediate following METH exposure.	Methamphetamine	153-157	programmed cell death 1	Sus scrofa	86-90
26330898-7	2015	We found that astrocytes expressed moderate levels of endogenous PD-1/PD-L1, which was diminished by METH exposure.	Methamphetamine	101-105	programmed cell death 1	Sus scrofa	65-69
26330898-8	2015	Our findings show a differential expression of PD-1/PD-L1 in neuroimmune cells in response to METH stimulation, suggesting that PD-1/PD-L1 interplay in these cell types could orchestrate the intercellular interactive communication for neuronal death or protection in the brain environment.	Methamphetamine	94-98	programmed cell death 1	Sus scrofa	47-51
26330898-8	2015	Our findings show a differential expression of PD-1/PD-L1 in neuroimmune cells in response to METH stimulation, suggesting that PD-1/PD-L1 interplay in these cell types could orchestrate the intercellular interactive communication for neuronal death or protection in the brain environment.	Methamphetamine	94-98	programmed cell death 1	Sus scrofa	128-132