PD-1/PD-L1 blockade

Where the papers sit

23 papers from the last 6 months study PD-1/PD-L1 blockade directly · updated from PubMed 12 Oct 2026

• Cancer Immunotherapy Response

  Cancer immunotherapy is moving toward biomarker-guided combinations that improve response depth and overcome suppressive microenvironments. Peripheral T-cell subsets, blood-based kinase activity, and response depth are being developed for efficacy or progression-risk assessment. Tregs, FN1+ macrophages, lactate-HMGB1 signaling, and TAMs recur as mechanisms of resistance across tumor types. Axitinib with survivin vaccination, berberine, PD-1-targeted IL-15, and TAM-directed nanotherapy represent attempts to convert refractory disease into responsive disease.

  11 papers · 47.8%

• Tumor Immune Checkpoint Biology

  Checkpoint blockade is being extended with local adjuvants, engineered delivery systems, and combination immune modulation. Bicarbonate potentiates PD-1 blockade in hepatocellular carcinoma, while copper complexes and exosome platforms target PD-L1 delivery or monitoring. Myeloma studies retain PD-1/PD-L1 biology as a central theme, alongside CTLA-4 and TNFRSF9 signaling. Regulatory T-cell dysfunction remains a caution, suggesting that stronger blockade may also create immunosuppressive escape states.

  5 papers · 21.7%

• PD-1 in Immune Homeostasis

  PD-1/PD-L1 signaling is being studied as a regulator of immune balance beyond cancer, particularly in sepsis, heart homeostasis, and invasive fungal infection. Myeloid PD-1/PD-L1 activity may protect adult cardiac homeostasis, whereas excessive signaling contributes to late-stage immunosuppression. Artificial exosomes and moxibustion aim to restore sepsis immunity while altering neutrophil fate or blocking PD-1/PD-L1. Anti-PD-1 with IFN-γ is emerging as adjunctive infection therapy, but the therapeutic window between immune recovery and tissue injury remains open.

  4 papers · 17.4%

• Mechanisms of PD-1 Resistance

  PD-1 resistance is being approached through alternative receptor binding, rational combinations, and disruption of tumor-cell immune-evasion programs. Engineered VHH domains and bispecific strategies seek to improve checkpoint targeting, while ERAP1, LILRB1, and KIR-related pathways provide additional resistance mechanisms or targets. β-catenin palmitoyl-switch activity links ferroptosis resistance with PD-L1-mediated immunosuppression. The direction is toward multi-node intervention rather than relying on pembrolizumab or nivolumab alone, especially in rare or refractory cancers.

  3 papers · 13%