Infectious diseases, autoantibodies, and autoimmunity
Infectious diseases, autoantibodies, and autoimmunity
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DOI：
10.1016/j.jaut.2022.102962
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发表时间：
2023-06-15
影响因子：
12.8
通讯作者：
Jiang，Wei
中科院分区：
文献类型：
--
作者：
Johnson，Douglas;Jiang，Wei
已知感染会引发人类自身免疫性疾病的爆发，并作为动物自身免疫性的煽动原因。有证据表明，感染在触发抗原特异性自身免疫中的致病作用，以前认为主要是通过抗原模拟。然而，感染可诱导旁观者自身反应性T和B细胞多克隆活化，据信导致非致病性和致病性自身免疫应答。最后，自身免疫中的表位扩散是由感染诱导的自身反应性细胞的表位变化的机制，促进了额外的自身表位的靶向。本文综述了最近的研究结果，强调感染介导的自身免疫反应，并讨论了可能的机制。
Infections are known to trigger flares of autoimmune diseases in humans and serve as an inciting cause of autoimmunity in animals. Evidence suggests a causative role of infections in triggering antigen-specific autoimmunity, previous thought mainly through antigen mimicry. However, an infection can induce bystander autoreactive T and B cell polyclonal activation, believed to result in non-pathogenic and pathogenic autoimmune responses. Lastly, epitope spreading in autoimmunity is a mechanism of epitope changes of autoreactive cells induced by infection, promoting the targeting of additional self-epitopes. This review highlights recent research findings, emphasizes infection-mediated autoimmune responses, and discusses the possible mechanisms involved.