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

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...

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Veröffentlicht in:Clinical microbiology reviews Jg. 19; H. 1; S. 80
Hauptverfasser: Fujinami, Robert S, von Herrath, Matthias G, Christen, Urs, Whitton, J Lindsay
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States 01.01.2006
Schlagworte:
Animals
Autoimmune Diseases - etiology
Autoimmune Diseases - immunology
Bystander Effect - immunology
Female
Humans
Lymphocyte Activation
Mice
Molecular Mimicry - immunology
T-Lymphocytes - immunology
Virus Diseases - complications
Viruses - growth & development
ISSN:0893-8512
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Zusammenfassung: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 persistence. 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-medicated diseases often linked with virus infections.
Bibliographie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
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ISSN:0893-8512
DOI:10.1128/CMR.19.1.80-94.2006