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Molecular mimicry, bystander activation, or viral persistence: Infections and autoimmune disease

期刊

CLINICAL MICROBIOLOGY REVIEWS
卷 19, 期 1, 页码 80-+

出版社

AMER SOC MICROBIOLOGY
DOI: 10.1128/CMR.19.1.80-94.2006

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资金

  1. NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI042314, P01AI058105] Funding Source: NIH RePORTER
  2. NIAID NIH HHS [P01 AI058105, R01 AI042314, R01 AI-42314, P01 AI-58105] Funding Source: Medline

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Virus infections and autoimmune disease have long been linked. These infections often precede the occurrence of inflammation in the target organ. Several mechanisms often used to explain the association of autoimmunity and virus infection are molecular mimicry, bystander activation (with or without epitope spreading), and viral persistance. These mechanisms have been used separately or in various combinations to account for the immunopathology observed at the site of infection and/or sites of autoimmune disease, such as the brain, heart, and pancreas. These mechanisms are discussed in the context of multiple sclerosis, myocarditis, and diabetes, three immune-mediated diseases often linked with virus infections.

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