Current evidence supports the concept that reactive arthritis (ReA) is an immune-mediated synovitis resulting from slow bacterial infections and showing intra-articular persistence of viable, non-culturable bacteria and/or immunogenetic bacterial antigens synthesized by metabolically active bacteria residing in the joint and/or elsewhere in the body. The mechanisms that lead to the development of ReA are complex and basically involve an interaction between an arthritogenic agent and a predisposed host. The way in which a host accommodates to invasive facultative intracellular bacteria is the key to the development of ReA. The details of the molecular pathways that explain the articular and extra-articular manifestations of the disease are still under investigation. Several studies have been done to gain a better understanding of the pathogenesis of ReA; these constitute the basis for a more rational therapeutic approach to this disease.

中文翻译：

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HLA-B27 相关反应性关节炎：发病机制和临床考虑。


目前的证据支持这样的概念：反应性关节炎 (ReA) 是一种由缓慢细菌感染引起的免疫介导的滑膜炎，并显示关节内持续存在活的、不可培养的细菌和/或由关节内代谢活跃的细菌合成的免疫遗传细菌抗原。和/或身体的其他地方。导致 ReA 发生的机制很复杂，基本上涉及致关节炎因子和易感宿主之间的相互作用。宿主适应侵入性兼性细胞内细菌的方式是 ReA 发展的关键。解释该疾病的关节和关节外表现的分子途径的细节仍在研究中。为了更好地了解 ReA 的发病机制，已经进行了多项研究；这些构成了对该疾病更合理的治疗方法的基础。