1. EGCG suppresses PD-1 expression of T cells via inhibiting NF-κB phosphorylation and nuclear translocation.
- Author
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Li ZD, Liu F, Zeng Y, Liu Y, Luo W, Yuan F, Li S, Li Q, Chen J, Fujita M, Zhang G, and Li Y
- Subjects
- Animals, Female, Humans, Mice, Apoptosis drug effects, Cell Line, Tumor, Mice, Inbred C57BL, Phosphorylation drug effects, Active Transport, Cell Nucleus drug effects, Catechin analogs & derivatives, Catechin pharmacology, NF-kappa B metabolism, Programmed Cell Death 1 Receptor metabolism, Programmed Cell Death 1 Receptor antagonists & inhibitors, T-Lymphocytes drug effects, T-Lymphocytes immunology, T-Lymphocytes metabolism
- 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., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)
- Published
- 2024
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