Infectious diseases and autoimmunity

被引:52
|
作者
Delogu, Lucia G. [2 ]
Deidda, Silvia [1 ]
Delitala, Giuseppe [1 ]
Manetti, Roberto [1 ]
机构
[1] Univ Sassari, Dept Clin Expt & Oncol Med, I-07100 Sassari, Italy
[2] Univ Sassari, Dept Drug Sci, I-07100 Sassari, Italy
来源
关键词
viral infection; bacterial infection; autoreactive lymphocyte; molecular mimicry; bystander activation; epitope spreading; autoimmune disease; MYELIN BASIC-PROTEIN; T-CELL-CLONES; MULTIPLE-SCLEROSIS PATIENTS; MOLECULAR MIMICRY; VIRAL-INFECTION; H+; K+-ADENOSINE TRIPHOSPHATASE; RHEUMATOID-ARTHRITIS; BYSTANDER ACTIVATION; PERNICIOUS-ANEMIA; VIRUS-INFECTION;
D O I
10.3855/jidc.2061
中图分类号
R51 [传染病];
学科分类号
100401 ;
摘要
Introduction: Autoimmunity occurs when the immune system recognizes and attacks host tissue. In addition to genetic factors, environmental triggers (in particular viruses, bacteria and other infectious pathogens) are thought to play a major role in the development of autoimmune diseases. Methodology: We searched PubMed, Cochrane, and Scopus without time limits for relevant articles. Results: In this review, we (i) describe the ways in which an infectious agent can initiate or exacerbate autoimmunity; (ii) discuss the evidence linking certain infectious agents to autoimmune diseases in humans; and (iii) describe the animal models used to study the link between infection and autoimmunity. Conclusions: Besides genetic predisposition to autoimmunity, viral and bacterial infections are known to be involved in the initiation and promotion of autoimmune diseases. These studies suggest that pathogens can trigger autoimmunity through molecular mimicry and their adjuvant effects during initiation of disease, and can promote autoimmune responses through bystander activation or epitope spreading via inflammation and/or superantigens.
引用
收藏
页码:679 / 687
页数:9
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