Toll-like receptors (TLR) that belong to the group of protein recognition receptor (PPR) provide an innate immune response following the sensing of conserved pathogen-associated microbial patterns (PAMPs) and changes in danger-associated molecular patterns (DAMPs) that are generated as a consequence of cellular injury. Analysis of the TLR pathway has moreover offered new insights into the pathogenesis of rheumatoid arthritis (RA). Indeed, a dysfunctional TLR-mediated response characterizes RA patients and participates in establishment of a chronic inflammatory state. Such an inappropriate TLR response has been attributed (i) to the report of important alterations in the microbiota and abnormal responses to infectious agents as part of RA; (ii) to the abnormal presence of TLR-ligands in the serum and synovial fluid of RA patients; (iii) to the overexpression of TLR molecules; (iv) to the production of a large panel of pro-inflammatory cytokines downstream of the TLR pathway; and (v) to genetic variants and epigenetic factors in susceptible RA patients promoting a hyper TLR response. As a consequence, the development of promising therapeutic strategies targeting TLRs for the treatment and prevention of RA is emerging.

中文翻译：

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类似收费的受体，感染和类风湿关节炎。

属于蛋白质识别受体（PPR）的Toll样受体（TLR）在感知到保守的病原体相关微生物模式（PAMPs）和危险相关分子模式（DAMPs）发生变化后提供先天免疫应答由于细胞损伤而产生的。此外，TLR途径的分析为类风湿关节炎（RA）的发病机理提供了新的见解。实际上，功能失调的TLR介导的反应是RA患者的特征，并参与了慢性炎症状态的建立。这种不适当的TLR反应归因于（i）有关微生物群重要变化和对作为RA一部分的传染原的异常反应的报道；（ii）RA患者血清和滑液中TLR配体的异常存在；（iii）TLR分子的过度表达；（iv）在TLR途径下游产生大量促炎细胞因子；（v）易感RA患者中的遗传变异和表观遗传因素，促进了高TLR反应。结果，正在出现针对TLR以治疗和预防RA的有前途的治疗策略。