Infectious agents can trigger autoimmune responses in a number of chronic inflammatory diseases. Lyme arthritis, which is caused by the tick-transmitted spirochaete Borrelia burgdorferi, is effectively treated in most patients with antibiotic therapy; however, in a subset of patients, arthritis can persist and worsen after the spirochaete has been killed (known as post-infectious Lyme arthritis). This Review details the current understanding of the pathogenetic events in Lyme arthritis, from initial infection in the skin, through infection of the joints, to post-infectious chronic inflammatory arthritis. The central feature of post-infectious Lyme arthritis is an excessive, dysregulated pro-inflammatory immune response during the infection phase that persists into the post-infectious period. This response is characterized by high amounts of IFNγ and inadequate amounts of the anti-inflammatory cytokine IL-10. The consequences of this dysregulated pro-inflammatory response in the synovium include impaired tissue repair, vascular damage, autoimmune and cytotoxic processes, and fibroblast proliferation and fibrosis. These synovial characteristics are similar to those in other chronic inflammatory arthritides, including rheumatoid arthritis. Thus, post-infectious Lyme arthritis provides a model for other chronic autoimmune or autoinflammatory arthritides in which complex immune responses can be triggered and shaped by an infectious agent in concert with host genetic factors.

传染性病原体可以在许多慢性炎症性疾病中引发自身免疫反应。莱姆关节炎，由蜱传播的螺旋体伯氏疏螺旋体引起, 在大多数接受抗生素治疗的患者中得到有效治疗；然而，在一部分患者中，关节炎会在螺旋体被杀死后持续存在并恶化（称为感染后莱姆关节炎）。这篇综述详细介绍了目前对莱姆关节炎发病事件的理解，从最初的皮肤感染，到关节感染，再到感染后慢性炎症性关节炎。感染后莱姆关节炎的主要特征是在感染阶段持续到感染后阶段的过度、失调的促炎免疫反应。这种反应的特点是大量的 IFNγ 和不足量的抗炎细胞因子 IL-10。滑膜中这种失调的促炎反应的后果包括组织修复受损，血管损伤、自身免疫和细胞毒性过程以及成纤维细胞增殖和纤维化。这些滑膜特征类似于其他慢性炎症性关节炎，包括类风湿性关节炎。因此，感染后莱姆关节炎为其他慢性自身免疫性或自身炎症性关节炎提供了一个模型，其中复杂的免疫反应可以由感染因子与宿主遗传因素共同触发和形成。