自身抗原特异性转化生长因子β诱导的Foxp3 +调节性T细胞通过抑制树突状细胞激活自身反应性T细胞来预防自身免疫。

Autoantigen-specific TGFbeta-induced Foxp3+ regulatory T cells prevent autoimmunity by inhibiting dendritic cells from activating autoreactive T cells.

作者信息

DiPaolo Richard J, Brinster Carine, Davidson Todd S, Andersson John, Glass Deborah, Shevach Ethan M

机构信息

Cellular Immunology Section, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.

出版信息

J Immunol. 2007 Oct 1;179(7):4685-93. doi: 10.4049/jimmunol.179.7.4685.

Abstract

Several strategies are being designed to test the therapeutic potential of Ag-specific regulatory T cells to prevent or treat autoimmune diseases. In this study, we demonstrate that naive CD4+ Foxp3- T cells specific for a naturally expressed autoantigen (H+/K+ ATPase) can be converted to Foxp3+ T regulatory cells (Tregs) when stimulated in presence of TGFbeta. TGFbeta-induced Tregs (iTregs) have all the characteristics of naturally generated regulatory T cells in vitro, and more importantly, are effective at preventing organ-specific autoimmunity in a murine model of autoimmune gastritis. H+/K+ ATPase specific iTregs were able to inhibit the initial priming and proliferation of autoreactive T cells, and appear to do so by acting on H+/K+ ATPase presenting dendritic cells (DC). DC exposed to iTregs in vivo were reduced in their ability to stimulate proliferation and cytokine production by H+/K+ ATPase specific T cells. iTregs specifically reduced CD80 and CD86 expression on the surface of H+/K+ ATPase presenting DC in vitro. These studies reveal the therapeutic potential of Ag specific iTregs to prevent autoimmunity, and provide a mechanism by which this population of regulatory T cells, and perhaps others, mediate their suppressive effects in vivo.

摘要

目前正在设计多种策略来测试抗原特异性调节性T细胞预防或治疗自身免疫性疾病的治疗潜力。在本研究中,我们证明,当在转化生长因子β(TGFβ)存在的情况下受到刺激时,对天然表达的自身抗原(H+/K+ATP酶)具有特异性的初始CD4+Foxp3-T细胞可转化为Foxp3+调节性T细胞(Tregs)。TGFβ诱导的Tregs(iTregs)在体外具有天然产生的调节性T细胞的所有特征,更重要的是,在自身免疫性胃炎的小鼠模型中能有效预防器官特异性自身免疫。H+/K+ATP酶特异性iTregs能够抑制自身反应性T细胞的初始致敏和增殖,并且似乎是通过作用于呈递H+/K+ATP酶的树突状细胞(DC)来实现的。在体内暴露于iTregs的DC刺激H+/K+ATP酶特异性T细胞增殖和产生细胞因子的能力降低。iTregs在体外特异性降低了呈递H+/K+ATP酶的DC表面的CD80和CD86表达。这些研究揭示了抗原特异性iTregs预防自身免疫的治疗潜力,并提供了这一调节性T细胞群体以及可能其他调节性T细胞群体在体内介导其抑制作用的机制。

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