A study by Pianta et al published in the Journal of Clinical Investigation provides new evidence that the pathogenesis of rheumatoid arthritis (RA) may involve molecular mimicry, one of the most venerable models for the aetiology of rheumatic disease.1 Molecular mimicry represents the development of cross-reactive B or T cell responses to a component of an infecting agent. As shown in this study, the agent in question may be a commensal in the gut microbiome rather than a bacterium or virus inducing clinical disease. While a violation of tolerance, molecular mimicry can occur due to the sharing of amino sequences by proteins from pathogen and host. If an immune response during infection goes awry, autoreactivity to the shared sequence can ensue. The most dramatic example of molecular mimicry is acute rheumatic fever (ARF), still a major problem worldwide. The scenario is now classic: within weeks of an infection with group A Streptococcus , usually pharyngitis, an inflammatory syndrome encompassing arthritis strikes a susceptible person. In ARF, the infection is obvious; the culprit bacterial antigen is the M protein.2 In a novel approach to finding molecular mimics, Pianta et al …

中文翻译：

---

肠道如何使关节发炎

Pianta 等人发表在《临床调查杂志》上的一项研究提供了新的证据，表明类风湿性关节炎 (RA) 的发病机制可能涉及分子模拟，这是风湿病病因学最古老的模型之一。 1 分子模拟代表了类风湿性关节炎 (RA) 的发展对感染因子成分的交叉反应性 B 或 T 细胞反应。如本研究所示，所讨论的病原体可能是肠道微生物组中的共生体，而不是引起临床疾病的细菌或病毒。虽然违反耐受性，但由于来自病原体和宿主的蛋白质共享氨基酸序列，可能会发生分子模拟。如果感染期间的免疫反应出现问题，就会发生对共享序列的自身反应。分子拟态最引人注目的例子是急性风湿热（ARF），仍然是世界范围内的一个主要问题。现在的情况很经典：在感染 A 组链球菌（通常是咽炎）后的几周内，一种包括关节炎的炎症综合征会袭击易感人群。在 ARF 中，感染是明显的；罪魁祸首细菌抗原是 M 蛋白。 2 在寻找分子模拟物的新方法中，Pianta 等人……