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树突状细胞通过Toll途径依赖性方式阻断CD4+CD25+ T细胞介导的抑制作用。

Toll pathway-dependent blockade of CD4+CD25+ T cell-mediated suppression by dendritic cells.

作者信息

Pasare Chandrashekhar, Medzhitov Ruslan

机构信息

Howard Hughes Medical Institute and Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.

出版信息

Science. 2003 Feb 14;299(5609):1033-6. doi: 10.1126/science.1078231. Epub 2003 Jan 16.

Abstract

Toll-like receptors (TLRs) control activation of adaptive immune responses by antigen-presenting cells (APCs). However, initiation of adaptive immune responses is also controlled by regulatory T cells (TR cells), which act to prevent activation of autoreactive T cells. Here we describe a second mechanism of immune induction by TLRs, which is independent of effects on costimulation. Microbial induction of the Toll pathway blocked the suppressive effect of CD4+CD25+ TR cells, allowing activation of pathogen-specific adaptive immune responses. This block of suppressor activity was dependent in part on interleukin-6, which was induced by TLRs upon recognition of microbial products.

摘要

Toll样受体(TLRs)通过抗原呈递细胞(APCs)控制适应性免疫反应的激活。然而,适应性免疫反应的启动也受到调节性T细胞(TR细胞)的控制,TR细胞的作用是防止自身反应性T细胞的激活。在此,我们描述了TLRs诱导免疫的第二种机制,该机制独立于对共刺激的影响。Toll途径的微生物诱导阻断了CD4+CD25+TR细胞的抑制作用,从而使病原体特异性适应性免疫反应得以激活。这种抑制活性的阻断部分依赖于白细胞介素-6,它是TLRs在识别微生物产物时所诱导产生的。

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