Retrovirus-associated rheumatic syndromes
The influence of environmental factors in the initiation of autoimmune rheumatic diseases is still under debate. Infections with viruses (eg, retroviruses) or expression of gene products encoded by endogenous retroviruses are believed to contribute to both loss of tolerance for autoantigens and immu...
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| Veröffentlicht in: | Current opinion in rheumatology 1998-07, Vol.10 (4), p.347-354 |
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| container_title | Current opinion in rheumatology |
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| creator | Herrmann, Martin Neidhart, Michel Gay, Steffen Hagenhofer, Manuela Kalden, Joachim R |
| description | The influence of environmental factors in the initiation of autoimmune rheumatic diseases is still under debate. Infections with viruses (eg, retroviruses) or expression of gene products encoded by endogenous retroviruses are believed to contribute to both loss of tolerance for autoantigens and immunosuppression. In various rheumatic disorders the detection of retroviral antibodies provides evidence for retroviral gene expression and suggests a role in the etiopathogenesis. Molecular mimicry, defects in apoptosis, altered autoantigens, and alterations of monocyte or macrophage as well as dendritic cell functions may contribute to the molecular mechanisms causing the loss of tolerance. On the other hand, destruction of lymphocytes during lytic retrovirus infections as well as envelope gene-env derived immunosuppressive retroviral gene products may prevent chronic inflammatory diseases and tissue destruction. Furthermore, retrovirus encoded superantigens with the potency to skew the T-cell repertoire may seriously modify the hostʼs immune system. |
| doi_str_mv | 10.1097/00002281-199807000-00012 |
| format | Article |
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Infections with viruses (eg, retroviruses) or expression of gene products encoded by endogenous retroviruses are believed to contribute to both loss of tolerance for autoantigens and immunosuppression. In various rheumatic disorders the detection of retroviral antibodies provides evidence for retroviral gene expression and suggests a role in the etiopathogenesis. Molecular mimicry, defects in apoptosis, altered autoantigens, and alterations of monocyte or macrophage as well as dendritic cell functions may contribute to the molecular mechanisms causing the loss of tolerance. On the other hand, destruction of lymphocytes during lytic retrovirus infections as well as envelope gene-env derived immunosuppressive retroviral gene products may prevent chronic inflammatory diseases and tissue destruction. 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| source | MEDLINE; Journals@Ovid Complete |
| subjects | Acquired Immunodeficiency Syndrome - complications AIDS/HIV Animals Disease Models, Animal Humans Retroviridae Infections - complications Rheumatic Diseases - complications Rheumatic Diseases - immunology Rheumatic Diseases - virology |
| title | Retrovirus-associated rheumatic syndromes |
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