The Kennedy Institute of Rheumatology, Imperial College London, 65 Aspenlea Road, London W6 8LH, UK.
Nat Rev Rheumatol. 2010 Dec;6(12):727-30. doi: 10.1038/nrrheum.2010.139. Epub 2010 Sep 7.
Autoimmunity in rheumatoid arthritis (RA) is characterized by an antibody response to citrullinated proteins. Two of the risk factors for RA-HLA-DRB1 shared epitope alleles and smoking-are also associated with periodontitis, which is largely, but not exclusively, caused by Porphyromonas gingivalis infection. Furthermore, RA and periodontitis have a similar pathophysiology, characterized by destructive inflammation. The citrullination of proteins by P. gingivalis and the subsequent generation of autoantigens that drive autoimmunity in RA represents a possible causative link between these two diseases. Antibodies directed towards the immunodominant epitope of human citrullinated α-enolase cross-react with a conserved sequence on citrullinated P. gingivalis enolase. On the basis of this cross-reactivity, in this Perspectives article we explore the hypothesis of molecular mimicry in the etiology of RA, with citrullinated enolase as the specific antigen involved.
类风湿关节炎 (RA) 的自身免疫特征为针对瓜氨酸化蛋白的抗体反应。RA 的两个风险因素——HLA-DRB1 共享表位等位基因和吸烟——也与牙周炎相关，而牙周炎主要（但并非完全）由牙龈卟啉单胞菌感染引起。此外，RA 和牙周炎具有相似的病理生理学特征，表现为破坏性炎症。牙龈卟啉单胞菌对蛋白质的瓜氨酸化以及随后产生的驱动 RA 自身免疫的自身抗原代表了这两种疾病之间可能的因果联系。针对人源瓜氨酸化α-烯醇酶免疫显性表位的抗体与瓜氨酸化牙龈卟啉单胞菌烯醇酶上的保守序列发生交叉反应。基于这种交叉反应，在本文的观点部分，我们探讨了 RA 病因学中分子模拟的假说，瓜氨酸化烯醇酶是涉及的特定抗原。
