The role of Toll-like receptor signalling in the pathogenesis of arthritis

被引：177

作者：

Brentano, F ^{[1
]}

Kyburz, D ^{[1
]}

Schorr, O ^{[1
]}

Gay, R ^{[1
]}

Gay, S ^{[1
]}

机构：

[1] Univ Zurich Hosp, Ctr Expt Rheumatol, CH-8091 Zurich, Switzerland

来源：

CELLULAR IMMUNOLOGY | 2005年 / 233卷 / 02期

关键词：

TLR; innate immunity; rheumatoid arthritis;

D O I：

10.1016/j.cellimm.2005.04.018

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 [细胞生物学]; 090102 [作物遗传育种];

摘要：

Recent evidence highlighted the role of Toll-like receptors (TLRs) as key recognition structures of the innate immune system. The activation of TLRs initiates the production of inflammatory cytokines, chemokines, tissue destructive enzymes, and type I interferons. In addition, TLR signalling plays an important role in the activation and direction of the adaptive immune system by the upregulation of costimulatory molecules of antigen presenting cells. Considering the important role of TLR signalling as a critical link between innate and adaptive immunity it has been proposed that a dysregulation in TLR signalling might be associated with autoimmunity. In this review, recent studies on TLR signal transduction pathways activated by corresponding ligands are summarized and evidence for a possible role of TLR signalling in the pathogenesis of rheumatoid arthritis is discussed. (c) 2005 Elsevier Inc. All rights reserved.

引用

页码：90 / 96

页数：7

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