PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 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 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 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 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 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 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 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 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 76-79 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 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 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 32184441-3 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 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 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 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 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 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 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 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<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 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 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 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 26330898-4 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 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