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Foxp3 + CD25 + CD4 + 自然调节性T细胞在显性自身耐受和自身免疫性疾病中的作用

Foxp3+ CD25+ CD4+ natural regulatory T cells in dominant self-tolerance and autoimmune disease.

作者信息

Sakaguchi Shimon, Ono Masahiro, Setoguchi Ruka, Yagi Haruhiko, Hori Shohei, Fehervari Zoltan, Shimizu Jun, Takahashi Takeshi, Nomura Takashi

机构信息

Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto, Japan.

出版信息

Immunol Rev. 2006 Aug;212:8-27. doi: 10.1111/j.0105-2896.2006.00427.x.

Abstract

Naturally arising CD25+ CD4+ regulatory T (Treg) cells, most of which are produced by the normal thymus as a functionally mature T-cell subpopulation, play key roles in the maintenance of immunologic self-tolerance and negative control of a variety of physiological and pathological immune responses. Natural Tregs specifically express Foxp3, a transcription factor that plays a critical role in their development and function. Complete depletion of Foxp3-expressing natural Tregs, whether they are CD25+ or CD25-, activates even weak or rare self-reactive T-cell clones, inducing severe and widespread autoimmune/inflammatory diseases. Natural Tregs are highly dependent on exogenously provided interleukin (IL)-2 for their survival in the periphery. In addition to Foxp3 and IL-2/IL-2 receptor, deficiency or functional alteration of other molecules, expressed by T cells or non-T cells, may affect the development/function of Tregs or self-reactive T cells, or both, and consequently tip the peripheral balance between the two populations toward autoimmunity. Elucidation of the molecular and cellular basis of this Treg-mediated active maintenance of self-tolerance will facilitate both our understanding of the pathogenetic mechanism of autoimmune disease and the development of novel methods of autoimmune disease prevention and treatment via enhancing and re-establishing Treg-mediated dominant control over self-reactive T cells.

摘要

自然产生的CD25 + CD4 +调节性T(Treg)细胞,其中大部分由正常胸腺产生,作为功能成熟的T细胞亚群,在维持免疫自身耐受性以及对各种生理和病理免疫反应的负调控中发挥关键作用。天然Treg特异性表达Foxp3,这是一种在其发育和功能中起关键作用的转录因子。完全耗尽表达Foxp3的天然Treg,无论它们是CD25 +还是CD25 -,都会激活即使是微弱或罕见的自身反应性T细胞克隆,引发严重且广泛的自身免疫/炎症性疾病。天然Treg在外周血中的存活高度依赖于外源性提供的白细胞介素(IL)-2。除了Foxp3和IL-2 / IL-2受体外,T细胞或非T细胞表达的其他分子的缺陷或功能改变,可能会影响Treg或自身反应性T细胞的发育/功能,或两者兼而有之,从而使这两种细胞在外周的平衡倾向于自身免疫。阐明这种Treg介导的自身耐受性主动维持的分子和细胞基础,将有助于我们理解自身免疫性疾病的发病机制,以及通过增强和重新建立Treg介导的对自身反应性T细胞的主导控制来开发预防和治疗自身免疫性疾病的新方法。

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