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Synergistic interaction between measles virus infection and myelin basic protein peptide-specific T cells in the induction of experimental allergic encephalomyelitis in Lewis rats
The questions how a viral infection induces cellular autoimmune reactions (CMAI) and which components of both virus and auto-antigen play part in this process were addressed in our animal model of measles virus (MV)-induced CMAI against myelin basic protein (MBP) during subacute measles encephalitis...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Published by Elsevier B.V.
1993
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7119583/ https://www.ncbi.nlm.nih.gov/pubmed/7689589 http://dx.doi.org/10.1016/0165-5728(93)90252-T |
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author | Liebert, Uwe G. ter Meulen, Volker |
author_facet | Liebert, Uwe G. ter Meulen, Volker |
author_sort | Liebert, Uwe G. |
collection | PubMed |
description | The questions how a viral infection induces cellular autoimmune reactions (CMAI) and which components of both virus and auto-antigen play part in this process were addressed in our animal model of measles virus (MV)-induced CMAI against myelin basic protein (MBP) during subacute measles encephalitis (SAME). In an attempt to define whether cellular or humoral immune responses are involved in the occurrence of the autoimmune based disease process, Lewis rats were treated with different combinations of antibodies and T cells reactive with either MV and its structural proteins or MBP and MBP-peptides. The only treatment combination after which experimental allergic encephalomyelitis (EAE)-like disease and pathology developed was when non-encephalitogenic T cells reactive against residues 69–81 of MBP were adoptively transferred into MV-infected Lewis rats. The results of the study show that T cells which are non-encephalitogenic in the normal central nervous tissue are capable of inducing an allergic encephalomyelitis in animals with a viral infection involving the brain. |
format | Online Article Text |
id | pubmed-7119583 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1993 |
publisher | Published by Elsevier B.V. |
record_format | MEDLINE/PubMed |
spelling | pubmed-71195832020-04-08 Synergistic interaction between measles virus infection and myelin basic protein peptide-specific T cells in the induction of experimental allergic encephalomyelitis in Lewis rats Liebert, Uwe G. ter Meulen, Volker J Neuroimmunol Article The questions how a viral infection induces cellular autoimmune reactions (CMAI) and which components of both virus and auto-antigen play part in this process were addressed in our animal model of measles virus (MV)-induced CMAI against myelin basic protein (MBP) during subacute measles encephalitis (SAME). In an attempt to define whether cellular or humoral immune responses are involved in the occurrence of the autoimmune based disease process, Lewis rats were treated with different combinations of antibodies and T cells reactive with either MV and its structural proteins or MBP and MBP-peptides. The only treatment combination after which experimental allergic encephalomyelitis (EAE)-like disease and pathology developed was when non-encephalitogenic T cells reactive against residues 69–81 of MBP were adoptively transferred into MV-infected Lewis rats. The results of the study show that T cells which are non-encephalitogenic in the normal central nervous tissue are capable of inducing an allergic encephalomyelitis in animals with a viral infection involving the brain. Published by Elsevier B.V. 1993-07 2002-12-10 /pmc/articles/PMC7119583/ /pubmed/7689589 http://dx.doi.org/10.1016/0165-5728(93)90252-T Text en Copyright © 1993 Published by Elsevier B.V. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active. |
spellingShingle | Article Liebert, Uwe G. ter Meulen, Volker Synergistic interaction between measles virus infection and myelin basic protein peptide-specific T cells in the induction of experimental allergic encephalomyelitis in Lewis rats |
title | Synergistic interaction between measles virus infection and myelin basic protein peptide-specific T cells in the induction of experimental allergic encephalomyelitis in Lewis rats |
title_full | Synergistic interaction between measles virus infection and myelin basic protein peptide-specific T cells in the induction of experimental allergic encephalomyelitis in Lewis rats |
title_fullStr | Synergistic interaction between measles virus infection and myelin basic protein peptide-specific T cells in the induction of experimental allergic encephalomyelitis in Lewis rats |
title_full_unstemmed | Synergistic interaction between measles virus infection and myelin basic protein peptide-specific T cells in the induction of experimental allergic encephalomyelitis in Lewis rats |
title_short | Synergistic interaction between measles virus infection and myelin basic protein peptide-specific T cells in the induction of experimental allergic encephalomyelitis in Lewis rats |
title_sort | synergistic interaction between measles virus infection and myelin basic protein peptide-specific t cells in the induction of experimental allergic encephalomyelitis in lewis rats |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7119583/ https://www.ncbi.nlm.nih.gov/pubmed/7689589 http://dx.doi.org/10.1016/0165-5728(93)90252-T |
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