Brentano Fabia, Kyburz Diego, Schorr Olivier, Gay Renate, Gay Steffen
Center of Experimental Rheumatology, University Hospital, CH-8091 Zurich, Switzerland.
Cell Immunol. 2005 Feb;233(2):90-6. doi: 10.1016/j.cellimm.2005.04.018.
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.
近期证据突显了Toll样受体(TLRs)作为先天性免疫系统关键识别结构的作用。TLRs的激活引发炎性细胞因子、趋化因子、组织破坏酶和I型干扰素的产生。此外,TLR信号传导通过上调抗原呈递细胞的共刺激分子,在适应性免疫系统的激活和定向中发挥重要作用。鉴于TLR信号传导作为先天性免疫和适应性免疫之间关键联系的重要作用,有人提出TLR信号传导失调可能与自身免疫有关。在本综述中,总结了关于相应配体激活的TLR信号转导途径的近期研究,并讨论了TLR信号传导在类风湿性关节炎发病机制中可能作用的证据。