Infectious diseases, autoantibodies, and autoimmunity

被引:14
|
作者
Johnson, Douglas [1 ,2 ]
Jiang, Wei [1 ,2 ,3 ,4 ]
机构
[1] Med Univ South Carolina, Dept Microbiol & Immunol, 173 Ashley Ave, Charleston, SC USA
[2] Ralph H Johnson VA Med Ctr, Charleston, SC USA
[3] Med Univ South Carolina, Dept Med, Divison Infect Dis, Charleston, SC USA
[4] 173 Ashley Ave,BSB214C, Charleston, SC 29425 USA
基金
美国国家卫生研究院;
关键词
Autoimmunity; Infectious disease; Molecular mimicry; Microbes; Autoantibodies; Bystander activation; SYSTEMIC-LUPUS-ERYTHEMATOSUS; EPSTEIN-BARR-VIRUS; HENOCH-SCHONLEIN PURPURA; CENTRAL-NERVOUS-SYSTEM; IFN-ALPHA PRODUCTION; HEAT-SHOCK PROTEINS; B-CELL RESPONSES; MULTIPLE-SCLEROSIS; ANTIPHOSPHOLIPID ANTIBODIES; RHEUMATOID-ARTHRITIS;
D O I
10.1016/j.jaut.2022.102962
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页数:13
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