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Anti I-A antibody suppresses active encephalomyelitis: treatment model for diseases linked to IR genes

To test the clinical relevance of monoclonal anti-I-A antibody in autoimmune disease, we investigated the effects of such a therapy in acute and chronic relapsing experimental allergic encephalomyelitis (EAE) by instituting treatment after the onset of paralytic signs and following the clinical cour...

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Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1983
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2187382/
https://www.ncbi.nlm.nih.gov/pubmed/6194246
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description To test the clinical relevance of monoclonal anti-I-A antibody in autoimmune disease, we investigated the effects of such a therapy in acute and chronic relapsing experimental allergic encephalomyelitis (EAE) by instituting treatment after the onset of paralytic signs and following the clinical course. In chronic relapsing EAE, animals treated with anti-I-As antibody had no mortality and fewer relapses when compared with control animals. Antibody levels to myelin basic protein were lower and histopathology showed milder lesions in the treated group. Similarly, in the acute EAE model, animals treated with anti-I-As antibody showed a dramatic reversal of paralytic signs and a rapid recovery. The mechanisms of action of antibody to IR gene products in autoimmune disease are discussed.
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spelling pubmed-21873822008-04-17 Anti I-A antibody suppresses active encephalomyelitis: treatment model for diseases linked to IR genes J Exp Med Articles To test the clinical relevance of monoclonal anti-I-A antibody in autoimmune disease, we investigated the effects of such a therapy in acute and chronic relapsing experimental allergic encephalomyelitis (EAE) by instituting treatment after the onset of paralytic signs and following the clinical course. In chronic relapsing EAE, animals treated with anti-I-As antibody had no mortality and fewer relapses when compared with control animals. Antibody levels to myelin basic protein were lower and histopathology showed milder lesions in the treated group. Similarly, in the acute EAE model, animals treated with anti-I-As antibody showed a dramatic reversal of paralytic signs and a rapid recovery. The mechanisms of action of antibody to IR gene products in autoimmune disease are discussed. The Rockefeller University Press 1983-10-01 /pmc/articles/PMC2187382/ /pubmed/6194246 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Articles
Anti I-A antibody suppresses active encephalomyelitis: treatment model for diseases linked to IR genes
title Anti I-A antibody suppresses active encephalomyelitis: treatment model for diseases linked to IR genes
title_full Anti I-A antibody suppresses active encephalomyelitis: treatment model for diseases linked to IR genes
title_fullStr Anti I-A antibody suppresses active encephalomyelitis: treatment model for diseases linked to IR genes
title_full_unstemmed Anti I-A antibody suppresses active encephalomyelitis: treatment model for diseases linked to IR genes
title_short Anti I-A antibody suppresses active encephalomyelitis: treatment model for diseases linked to IR genes
title_sort anti i-a antibody suppresses active encephalomyelitis: treatment model for diseases linked to ir genes
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2187382/
https://www.ncbi.nlm.nih.gov/pubmed/6194246