Pasare Chandrashekhar, Medzhitov Ruslan
Howard Hughes Medical Institute and Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
Science. 2003 Feb 14;299(5609):1033-6. doi: 10.1126/science.1078231. Epub 2003 Jan 16.
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.
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。