TGF-β对T细胞的调控。

IF 26.9 1区 医学 Q1 IMMUNOLOGY Annual review of immunology Pub Date : 2023-04-26 DOI:10.1146/annurev-immunol-101921-045939
WanJun Chen
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引用次数: 3

摘要

转化生长因子β (TGF-β)是调节T细胞发育、活化、增殖、分化和死亡的关键细胞因子。在CD4+ T细胞中,TGF-β维持静止并控制初始T细胞的激活。TGF-β在抑制Th1和Th2细胞的分化和功能的同时,促进Th17和Th9细胞的分化。TGF-β是诱导初始T细胞Foxp3和调节性T细胞发育所必需的。TGF-β在组织驻留记忆CD8+ T细胞的分化及其在组织中的保留中至关重要,而它抑制效应T细胞的功能。此外,TGF-β还调节自然杀伤T细胞、γδ T细胞、先天淋巴样细胞和肠道上皮内淋巴细胞的产生或功能。在这里,我强调了我们对TGF-β调节T细胞的理解的主要发现和最新进展,并提供了该领域的个人观点。
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TGF-β Regulation of T Cells.

Transforming growth factor β (TGF-β) is a key cytokine regulating the development, activation, proliferation, differentiation, and death of T cells. In CD4+ T cells, TGF-β maintains the quiescence and controls the activation of naive T cells. While inhibiting the differentiation and function of Th1 and Th2 cells, TGF-β promotes the differentiation of Th17 and Th9 cells. TGF-β is required for the induction of Foxp3 in naive T cells and the development of regulatory T cells. TGF-β is crucial in the differentiation of tissue-resident memory CD8+ T cells and their retention in the tissue, whereas it suppresses effector T cell function. In addition, TGF-β also regulates the generation or function of natural killer T cells, γδ T cells, innate lymphoid cells, and gut intraepithelial lymphocytes. Here I highlight the major findings and recent advances in our understanding of TGF-β regulation of T cells and provide a personal perspective of the field.

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来源期刊
Annual review of immunology
Annual review of immunology 医学-免疫学
CiteScore
57.20
自引率
0.70%
发文量
29
期刊介绍: The Annual Review of Immunology, in publication since 1983, focuses on basic immune mechanisms and molecular basis of immune diseases in humans. Topics include innate and adaptive immunity; immune cell development and differentiation; immune control of pathogens (viruses, bacteria, parasites) and cancer; and human immunodeficiency and autoimmune diseases. The current volume of this journal has been converted from gated to open access through Annual Reviews' Subscribe to Open program, with all articles published under a CC BY license.
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