EGCG suppresses PD-1 expression of T cells via inhibiting NF-κB phosphorylation and nuclear translocation

Int Immunopharmacol. 2024 May 30:133:112069. doi: 10.1016/j.intimp.2024.112069. Epub 2024 Apr 20.

Abstract

Epigallocatechin-3-gallate (EGCG) is an important tea polyphenol with anti-tumor potential. Our previous studies revealed that EGCG was a promising immune checkpoint inhibitor (ICI) as it could downregulate expression of programmed cell death 1 ligand 1 (PD-L1) in tumor cells, thereby resulting tumor killing effect. In particular, EGCG can effectively avoid the inflammatory storm caused by anti-tumor therapy, which is a healthy green capacity absent from many ICIs. However, the relationship between EGCG and programmed cell death 1 (PD-1) of T cells remains unclear. In this work, we explored the effect of EGCG on T cells and found that EGCG suppressed PD-1 via inhibiting NF-κB phosphorylation and nuclear translocation. Furtherly, the capability of EGCG was confirmed in tumor-bearing mice to inhibit PD-1 expression in T cells and enhance apoptosis in tumor cells. These results implied that EGCG could inhibit the expression of PD-1 in T cells, thereby promoting anti-tumor effects of T cells. EGCG will be a promising candidate in anti-tumor therapy.

Keywords: Anti-tumor; EGCG; NF-κB; PD-1; T cells.

MeSH terms

  • Active Transport, Cell Nucleus* / drug effects
  • Animals
  • Apoptosis / drug effects
  • Catechin* / analogs & derivatives
  • Catechin* / pharmacology
  • Cell Line, Tumor
  • Female
  • Humans
  • Mice
  • Mice, Inbred C57BL
  • NF-kappa B* / metabolism
  • Phosphorylation / drug effects
  • Programmed Cell Death 1 Receptor* / antagonists & inhibitors
  • Programmed Cell Death 1 Receptor* / metabolism
  • T-Lymphocytes* / drug effects
  • T-Lymphocytes* / immunology
  • T-Lymphocytes* / metabolism

Substances

  • Catechin
  • epigallocatechin gallate
  • NF-kappa B
  • Pdcd1 protein, mouse
  • Programmed Cell Death 1 Receptor