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Toll样受体与糖尿病。

Toll-like receptors and diabetes.

作者信息

Wong F Susan, Wen Li

机构信息

Department of Cellular and Molecular Medicine, School of Medical Sciences, University of Bristol, Bristol, UK.

出版信息

Ann N Y Acad Sci. 2008 Dec;1150:123-32. doi: 10.1196/annals.1447.063.

Abstract

Toll-like receptors (TLRs) recognize molecular patterns relating to a variety of microbial infections. Stimulation through TLRs leads to activation of antigen-presenting cells, production of inflammatory cytokines creating inflammation, and production of type 1 interferons (IFNs) that include IFN-alpha and -beta, and exerts direct effects on regulatory cells. These effects can direct the immune response, dealing with the immediate problems of infection and activating more specific responses of the adaptive immune system. However, it has recently been recognized that these receptors may recognize endogenous ligands that include DNA, RNA, and proteins that arise from cellular stress. This may have an effect on autoimmune responses in a number of ways, both activating and inhibitory. The means by which infection or endogenous stimuli through TLRs may influence autoimmunity will be discussed.

摘要

Toll样受体(TLRs)识别与多种微生物感染相关的分子模式。通过TLRs的刺激会导致抗原呈递细胞的激活、引发炎症的炎性细胞因子的产生、包括α干扰素和β干扰素在内的1型干扰素(IFNs)的产生,并对调节细胞产生直接影响。这些作用可引导免疫反应,处理感染的即时问题并激活适应性免疫系统更具特异性的反应。然而,最近人们认识到这些受体可能识别包括细胞应激产生的DNA、RNA和蛋白质在内的内源性配体。这可能以多种方式影响自身免疫反应,既有激活作用也有抑制作用。本文将讨论通过TLRs的感染或内源性刺激可能影响自身免疫的方式。

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