Lyme arthritis: linking infection, inflammation and autoimmunity.
Lyme arthritis: linking infection, inflammation and autoimmunity.
复制标题
DOI：
10.1038/s41584-021-00648-5
复制
发表时间：
2021-08
期刊：
影响因子：
--
通讯作者：
中科院分区：
文献类型：
--
作者：
感染性因子可在许多慢性炎症性疾病中引发自身免疫反应。莱姆病关节炎是由蜱传播的螺旋体伯氏疏螺旋体引起的，对大多数患者来说，抗生素治疗是有效的；然而，在一部分患者中，在螺旋体被杀死后，关节炎会持续存在并恶化（称为感染后莱姆病）。这篇综述详细介绍了目前对莱姆病发病事件的了解，从最初的皮肤感染，到关节感染，再到感染后的慢性炎症性关节炎。感染后莱姆病的中心特征是感染期过度的、失调的促炎免疫反应，这种反应持续到感染后时期。这种反应的特点是IFNγ含量高，而抗炎细胞因子IL-10含量不足。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性关节炎，包括类风湿关节炎。因此，感染后莱姆病为其他慢性自身免疫或自身炎症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协同触发和塑造。
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.
登录
查看更多内容
影响因子：
6.7
作者：
Casselli T;Divan A;Vomhof-DeKrey EE;Tourand Y;Pecoraro HL;Brissette CA
通讯作者：
Brissette CA
影响因子：
13.3
作者：
Bockenstedt, Linda K.;Wormser, Gary P.
通讯作者：
Wormser, Gary P.
影响因子：
24.8
作者：
Carmona-Rivera, Carmelo;Carlucci, Philip M.;Kaplan, Mariana J.
通讯作者：
Kaplan, Mariana J.
影响因子：
11.8
作者：
Cerar, Tjasa;Strle, Franc;Strle, Klemen
通讯作者：
Strle, Klemen
影响因子：
3.8
作者：
COMSTOCK, LE;THOMAS, DD
通讯作者：
THOMAS, DD