Engaging PD-1 rescuesregulatory T cell function and inhibits inflammatory T cells in rheumatoid arthritis

Clin Exp Immunol. 2025 Jan 21;219(1):uxaf035. doi: 10.1093/cei/uxaf035.

Abstract

Background: Despite their synovial enrichment, regulatory T cells (Treg) fail to alleviate the joint inflammation in rheumatoid arthritis (RA). This indicates their functional impairment in the synovial milieu of RA patients.

Results: Here, we demonstrate that a deficit in the PD-1 pathway incapacitates the synovial Treg cells, and engaging programmed cell death protein-1 (PD-1) restores their suppressive function (interleukin 10, transforming growth factor beta secretion), which in turn suppresses the synovial inflammatory T cells (IFN-γ+, IL-17+ TNF-α+). We also showed that a deficit in programmed death ligand-1 expression on RA synovial macrophages contributes to impaired Treg cell function.

Conclusion: Rejuvenating synovial Treg cell function via PD-1 engagement may be a potential strategy to ameliorate the synovial inflammation in RA patients.

Keywords: PD-1; RA; immunotherapy; regulatory T cells.

MeSH terms

  • Arthritis, Rheumatoid* / immunology
  • Arthritis, Rheumatoid* / pathology
  • B7-H1 Antigen / immunology
  • B7-H1 Antigen / metabolism
  • Female
  • Humans
  • Inflammation / immunology
  • Macrophages / immunology
  • Male
  • Middle Aged
  • Programmed Cell Death 1 Receptor* / immunology
  • Programmed Cell Death 1 Receptor* / metabolism
  • Synovial Membrane* / immunology
  • Synovial Membrane* / pathology
  • T-Lymphocytes, Regulatory* / immunology

Substances

  • Programmed Cell Death 1 Receptor
  • PDCD1 protein, human
  • B7-H1 Antigen