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Toll样受体——类风湿关节炎背后的强大驱动力。

Toll-like receptor--a potent driving force behind rheumatoid arthritis.

作者信息

Takagi Michiaki

机构信息

Department of Orthopaedic Surgery, Yamagata University School of Medicine, Japan.

出版信息

J Clin Exp Hematop. 2011;51(2):77-92. doi: 10.3960/jslrt.51.77.

DOI:10.3960/jslrt.51.77
PMID:22104306
Abstract

Toll like receptor (TLR), one of the key functions of innate immune system, can recognize not only exogenous pathogen-associated molecular patterns, namely PAMPs, but also endogenous molecules created upon tissue injury, sterile inflammation and degeneration. Endogenous TLR ligands are called as damage-associated molecular patters (DAMPs), including endogenous molecules released by activated and necrotic cells, and extracellular matrix molecules. DAMPs are also known as alarmins. TLR research has brought about new insights in the rheumatic diseases. Previous reports suggest that TLRs and the signal pathways intensively contribute to the pathogenesis of rheumatoid arthritis (RA) and other arthritic conditions with interaction of various TLR ligands. Accumulated knowledge of TLR system is summarized to overlook TLRs and the signaling pathway in arthritis conditions, with special reference to RA.

摘要

Toll样受体(TLR)是固有免疫系统的关键功能之一,不仅能够识别外源性病原体相关分子模式,即病原体相关分子模式(PAMP),还能识别组织损伤、无菌性炎症和变性时产生的内源性分子。内源性TLR配体被称为损伤相关分子模式(DAMP),包括活化和坏死细胞释放的内源性分子以及细胞外基质分子。DAMP也被称为警报素。TLR研究为风湿性疾病带来了新的见解。先前的报道表明,TLR及其信号通路通过各种TLR配体的相互作用,在类风湿关节炎(RA)和其他关节炎疾病的发病机制中发挥着重要作用。本文总结了TLR系统的相关知识,以审视关节炎疾病中的TLR及其信号通路,特别是RA。

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