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炎症性肠病的免疫发病机制:聚焦于组织驻留记忆T细胞。

Immunological pathogenesis of inflammatory bowel disease: focus on tissue resident memory T cells.

作者信息

Hu Jiayan, Wang Wenting, Wang Muyuan, Wu Chunye, Jiao Yao, Li Yitong, Zhang Wenji, Liang Chengtao, Lin Zhengdao, Yu Yitong, Li Junxiang, Mao Tangyou

机构信息

Dongfang Hospital, Beijing University of Chinese Medicine, Beijing, China.

Beijing University of Chinese Medicine, Beijing, China.

出版信息

Front Immunol. 2025 Jun 3;16:1591584. doi: 10.3389/fimmu.2025.1591584. eCollection 2025.

DOI:10.3389/fimmu.2025.1591584
PMID:40529369
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12170311/
Abstract

Tissue-resident memory T (T) cells are a type of tissue-restricted memory T cells with terminal differentiation and a memory function. They exist in mucosal tissues for a long period. In the absence of disease, T cells promote essential inflammation, which reinforces the intestinal barrier and prevents bacterial translocation. However, in inflammatory or autoimmune environments, T cells are hyperactivated. This heightened activity causes the host to release excessive pro-inflammatory cytokines, resulting in local immune imbalances and damage to the barrier, ultimately leading to tissue lesions. Numbers of studies have shown that T cells play a crucial role in the development and progression of inflammatory bowel disease (IBD), suggesting that targeted regulation of T cells homeostasis may be an important strategy for treating IBD. Here, we compiled the existing understanding of the role of T cells in IBD, with particular emphasis on the associated mechanisms and approaches for targeting T cells in IBD treatment. This review will serve as a foundation for a better understanding of IBD development and enhancing the effectiveness of clinical treatments for IBD.

摘要

组织驻留记忆T(T)细胞是一类具有终末分化和记忆功能的组织限制性记忆T细胞。它们长期存在于黏膜组织中。在没有疾病的情况下,T细胞促进必要的炎症反应,增强肠道屏障并防止细菌移位。然而,在炎症或自身免疫环境中,T细胞会过度活化。这种增强的活性导致宿主释放过多的促炎细胞因子,导致局部免疫失衡和屏障受损,最终导致组织损伤。大量研究表明,T细胞在炎症性肠病(IBD)的发生和发展中起关键作用,这表明靶向调节T细胞稳态可能是治疗IBD的重要策略。在此,我们汇总了对T细胞在IBD中作用的现有认识,特别强调了IBD治疗中靶向T细胞的相关机制和方法。本综述将为更好地理解IBD的发展及提高IBD临床治疗效果奠定基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1326/12170311/69753b2b7a7c/fimmu-16-1591584-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1326/12170311/3b63d0dff19d/fimmu-16-1591584-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1326/12170311/69753b2b7a7c/fimmu-16-1591584-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1326/12170311/3b63d0dff19d/fimmu-16-1591584-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1326/12170311/69753b2b7a7c/fimmu-16-1591584-g002.jpg

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T-bet deficiency and Hic1 induction override TGF-β-dependency in the formation of CD103 intestine-resident memory CD8 T cells.T-bet 缺陷和 Hic1 诱导可克服 TGF-β 依赖性,从而形成 CD103 肠道驻留记忆 CD8 T 细胞。
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