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Programmed cell death protein 1

Programmed cell death protein 1 (PD-1), encoded by PDCD1, is an inhibitory immune-checkpoint receptor expressed primarily on activated immune cells, including T cells.

Rebuilt from PubMed 18 Sept 2026 · no new papers today

Where the papers sit

19 papers study programmed cell death protein 1 directly. The themes below are drawn from those 19.

  • T-Cell Dysfunction and Resistance : Work is moving toward explaining checkpoint resistance through hypoxic neutrophils, metabolic reprogramming, S100A10-driven CD8-positive T-cell exhaustion, disrupted cytotoxic lysis, and altered PD-1 signaling. 7 papers · 36.8%

  • Immune Response in Carcinoma : Chemoimmunotherapy and chemoradiotherapy are being linked to CD8-positive T-cell activity, circulating cytokines, objective response, survival, and treatment-related adverse events across locally advanced carcinomas. 4 papers · 21.1%

  • PD-1 Therapy Biomarkers : Biomarker research spans tumor mechanics, plasma-cell immunotherapy targets, proteomic and metabolomic signatures of immune-related adverse events, and IKZF2/IKZF4 degradation to target regulatory T cells. 4 papers · 21.1%

  • PD-L1 Regulation and Targeting : PD-L1 research is expanding from expression and survival associations toward miRNA and PRKX-mediated regulation, structure-guided small-molecule inhibitors, and combination strategies involving TGFβ blockade and chemotherapy. 4 papers · 21.1%

Recent Findings on Programmed cell death protein 1

PD-1 Resistance and Immune Evasion: S100A10, PRKX, HIF1A+ CSF3R+ neutrophils, and LASP1 deficiency identify distinct routes to impaired anti-PD-1 responses across solid tumors 42732672Sep42716706Sep42711068Sep42686372Sep. S100A10 activates cPLA2-5-LOX-mediated arachidonic acid metabolism and ferroptosis-associated signaling, driving CD8+ T-cell exhaustion in hepatocellular carcinoma; its inhibition improves anti-PD-1 therapy. 42732672Sep PRKX phosphorylates PD-L1 at T285, recruits YWHAE, prevents UBE2M-mediated ubiquitination, and stabilizes PD-L1 in an immunosuppressive gastric cancer subtype 42716706Sep. In NSCLC, a hypoxic niche containing HIF1A+ CSF3R+ neutrophils, exhausted T cells, and stromal cells promotes senescence, glycolysis, and neoadjuvant therapy resistance; platycodin-D2, navitoclax, and anti-PD-1 improved tumor control in mice 42711068Sep. LASP1 deficiency instead disrupts Arp2/3-regulated cytoskeletal dynamics and lipid organization at the immunological synapse, while simvastatin restored anti-PD-1 sensitivity 42686372Sep. Conserved miRNAs and cancer-cell mechanical properties add candidate biomarkers, although miR-138-5p showed an opposite survival association from several other miRNAs, and tumor cell death trajectories varied by cell type 42616478Aug42535479Jul. QA9 extends this direction toward direct intervention by stabilizing the PD-L1 dimer while improving water solubility and adding antiangiogenic activity 42720488Sep.

Clinical Immunotherapy Outcomes: Tislelizumab, TP chemotherapy, and afatinib produced a 40.6% complete pathologic response rate, an 82.5% objective response rate, and a 97.3% 1-year overall survival rate in resectable locally advanced head and neck squamous cell carcinoma 42731876Sep. Increased intratumoral cytotoxic T lymphocytes and B cells were associated with pathologic response, while treatment increased peripheral CD8+ T cells and reduced B cells 42731876Sep. In pretreated metastatic triple-negative breast cancer, Trop-2 antibody-drug conjugates showed higher objective response rates and longer progression-free survival when combined with a PD-1 inhibitor, particularly with an added antiangiogenic agent, without increased severe toxicity 42714605Sep. Proteomic and metabolomic profiles linked immune-related adverse events after PD-1 blockade to NF-κB pathway involvement, altered SNRPA and CD63, an elevated kynurenine/tryptophan ratio, and lipid differences 42695906Sep. Plasma IL-10, CXCL9, CXCL13, sCD163, and soluble PD-1 tracked immune-desert, immune-excluded, and immune-inflamed phenotypes in head and neck squamous cell carcinoma, supporting biomarker-guided treatment and toxicity assessment 42684559Sep.

Tumor Immune Modulation: The PD-1 cytoplasmic domain directly inhibits T-cell receptor-induced LAT condensation through unphosphorylated tyrosines in its inhibitory motifs, whereas phosphorylation eliminates this inhibition 42721241Sep. BMS-986449 selectively degrades IKZF2 and IKZF4, suppresses tumors in humanized Cereblon knock-in mice, and produces stronger growth inhibition with anti-PD-1 therapy 42677819Sep. Oral bacterial membrane-hybridized nanovaccines use GP2-mediated M-cell transcytosis, dendritic cell reconfiguration, and CCR7-dependent trafficking to connect mucosal immunity with tumor control; PD-1 blockade further enhances effector mobilization and memory against rechallenge 42497859Jul. These approaches shift immune modulation toward signaling-condensate control, regulatory T-cell depletion, and mucosal-systemic vaccination alongside checkpoint inhibition.