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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| Vydáno v: | Clinical microbiology reviews Ročník 19; číslo 1; s. 80 |
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| Hlavní autoři: | , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
United States
01.01.2006
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| Témata: | |
| ISSN: | 0893-8512 |
| On-line přístup: | Zjistit podrobnosti o přístupu |
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| Abstract | 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. |
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| AbstractList | 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. 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.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. |
| Author | Fujinami, Robert S Christen, Urs von Herrath, Matthias G Whitton, J Lindsay |
| Author_xml | – sequence: 1 givenname: Robert S surname: Fujinami fullname: Fujinami, Robert S email: Robert.Fujinami@hsc.utah.edu organization: Department of Neurology, University of Utah School of Medicine, 30 N 1900 E, 3R330 SOM, Salt Lake City, UT 84132-2305, USA. Robert.Fujinami@hsc.utah.edu – sequence: 2 givenname: Matthias G surname: von Herrath fullname: von Herrath, Matthias G – sequence: 3 givenname: Urs surname: Christen fullname: Christen, Urs – sequence: 4 givenname: J Lindsay surname: Whitton fullname: Whitton, J Lindsay |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/16418524$$D View this record in MEDLINE/PubMed |
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| Snippet | Virus infections and autoimmune disease have long been linked. These infections often precede the occurrence of inflammation in the target organ. Several... |
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| SubjectTerms | 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 |
| Title | Molecular mimicry, bystander activation, or viral persistence: infections and autoimmune disease |
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