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辅助性 22 细胞在自身免疫性疾病发病机制中的作用。

Role of Th22 Cells in the Pathogenesis of Autoimmune Diseases.

机构信息

Department of Blood Transfusion, Shaoxing People's Hospital (Shaoxing Hospital, Zhejiang University School of Medicine), Shaoxing, China.

Department of Pathology and Shenzhen Institute of Research and Innovation, The University of Hong Kong; Chongqing International Institute for Immunology, Chongqing, China.

出版信息

Front Immunol. 2021 Jul 6;12:688066. doi: 10.3389/fimmu.2021.688066. eCollection 2021.

DOI:10.3389/fimmu.2021.688066
PMID:34295334
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8290841/
Abstract

Upon antigenic stimulation, naïve CD4T cells differentiate into different subsets and secrete various cytokines to exert biological effects. Th22 cells, a newly identified CD4T cell subset,are distinct from the Th1, Th2 and Th17 subsets. Th22 cells secrete certain cytokines such as IL-22, IL-13 and TNF-α, but not others, such as IL-17, IL-4, or interferon-γ (IFN-γ), and they express chemokine receptors CCR4, CCR6 and CCR10. Th22 cells were initially found to play a role in skin inflammatory diseases, but recent studies have demonstrated their involvement in the development of various autoimmune diseases. Here, we review research advances in the origin, characteristics and effector mechanisms of Th22 cells, with an emphasis on the role of Th22 cells and their main effector cytokine IL-22 in the pathogenesis of autoimmune diseases. The findings presented here may facilitate the development of new therapeutic strategies for targeting these diseases.

摘要

在抗原刺激下,幼稚 CD4T 细胞分化为不同亚群,并分泌各种细胞因子发挥生物学效应。Th22 细胞是新鉴定的 CD4T 细胞亚群,与 Th1、Th2 和 Th17 亚群不同。Th22 细胞分泌某些细胞因子,如 IL-22、IL-13 和 TNF-α,但不分泌其他细胞因子,如 IL-17、IL-4 或干扰素-γ(IFN-γ),并且它们表达趋化因子受体 CCR4、CCR6 和 CCR10。最初发现 Th22 细胞在皮肤炎症性疾病中发挥作用,但最近的研究表明它们参与了各种自身免疫性疾病的发生。在这里,我们综述了 Th22 细胞的起源、特征和效应机制的研究进展,重点介绍了 Th22 细胞及其主要效应细胞因子 IL-22 在自身免疫性疾病发病机制中的作用。这里提出的研究结果可能有助于为这些疾病开发新的靶向治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac2a/8290841/6dd2f723cf2b/fimmu-12-688066-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac2a/8290841/0d3607547106/fimmu-12-688066-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac2a/8290841/a11e8691173d/fimmu-12-688066-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac2a/8290841/6dd2f723cf2b/fimmu-12-688066-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac2a/8290841/0d3607547106/fimmu-12-688066-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac2a/8290841/a11e8691173d/fimmu-12-688066-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac2a/8290841/6dd2f723cf2b/fimmu-12-688066-g003.jpg

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