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细胞因子信号和共刺激分子对 Treg 细胞的调节。

Regulation of Treg cells by cytokine signaling and co-stimulatory molecules.

机构信息

School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, China.

Institute for Research and Continuing Education, Hong Kong Baptist University, Shenzhen, China.

出版信息

Front Immunol. 2024 May 13;15:1387975. doi: 10.3389/fimmu.2024.1387975. eCollection 2024.

DOI:10.3389/fimmu.2024.1387975
PMID:38807592
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11131382/
Abstract

CD4CD25Foxp3 regulatory T cells (Tregs), a vital component of the immune system, are responsible for maintaining immune homeostasis and preventing excessive immune responses. This review explores the signaling pathways of the cytokines that regulate Treg cells, including transforming growth factor beta (TGF-β), interleukin (IL)-2, IL-10, and IL-35, which foster the differentiation and enhance the immunosuppressive capabilities of Tregs. It also examines how, conversely, signals mediated by IL-6 and tumor necrosis factor -alpha (TNF-α) can undermine Treg suppressive functions or even drive their reprogramming into effector T cells. The B7 family comprises indispensable co-stimulators for T cell activation. Among its members, this review focuses on the capacity of CTLA-4 and PD-1 to regulate the differentiation, function, and survival of Tregs. As Tregs play an essential role in maintaining immune homeostasis, their dysfunction contributes to the pathogenesis of autoimmune diseases. This review delves into the potential of employing Treg-based immunotherapy for the treatment of autoimmune diseases, transplant rejection, and cancer. By shedding light on these topics, this article aims to enhance our understanding of the regulation of Tregs by cytokines and their therapeutic potential for various pathological conditions.

摘要

CD4+CD25+Foxp3+ 调节性 T 细胞(Tregs)是免疫系统的重要组成部分,负责维持免疫稳态和防止过度的免疫反应。本综述探讨了调节 Treg 细胞的细胞因子的信号通路,包括转化生长因子-β(TGF-β)、白细胞介素(IL)-2、IL-10 和 IL-35,它们促进 Treg 的分化并增强其免疫抑制功能。还研究了相反,IL-6 和肿瘤坏死因子-α(TNF-α)介导的信号如何破坏 Treg 的抑制功能,甚至驱动其重编程为效应 T 细胞。B7 家族是 T 细胞激活的不可或缺的共刺激分子。在其成员中,本综述重点关注 CTLA-4 和 PD-1 调节 Treg 的分化、功能和存活的能力。由于 Tregs 在维持免疫稳态中起着至关重要的作用,它们的功能障碍导致自身免疫性疾病的发病机制。本综述深入探讨了基于 Treg 的免疫疗法治疗自身免疫性疾病、移植排斥和癌症的潜力。通过探讨这些主题,本文旨在增强我们对细胞因子调节 Tregs 的理解及其在各种病理情况下的治疗潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0edd/11131382/42b7c94f8d20/fimmu-15-1387975-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0edd/11131382/176713ae2a9d/fimmu-15-1387975-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0edd/11131382/42b7c94f8d20/fimmu-15-1387975-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0edd/11131382/176713ae2a9d/fimmu-15-1387975-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0edd/11131382/42b7c94f8d20/fimmu-15-1387975-g002.jpg

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