An essential role of virus-infected B cells in the marmoset experimental autoimmune encephalomyelitis model

Infection with Epstein–Barr virus (EBV) has been associated with an enhanced risk of genetically susceptible individuals to develop multiple sclerosis (MS). However, an explanation for the contrast between the high EBV infection prevalence (60–90%) and the low MS prevalence (0.1%) eludes us. Here we...

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Detalles Bibliográficos
Autores principales: ’t Hart, Bert A, Kap, Yolanda S
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2017
Materias:
Review
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5466146/
https://www.ncbi.nlm.nih.gov/pubmed/28607749
http://dx.doi.org/10.1177/2055217317690184
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author ’t Hart, Bert A
Kap, Yolanda S
author_facet ’t Hart, Bert A
Kap, Yolanda S
author_sort ’t Hart, Bert A
collection PubMed
description Infection with Epstein–Barr virus (EBV) has been associated with an enhanced risk of genetically susceptible individuals to develop multiple sclerosis (MS). However, an explanation for the contrast between the high EBV infection prevalence (60–90%) and the low MS prevalence (0.1%) eludes us. Here we propose a new concept for the EBV–MS association developed in the experimental autoimmune encephalomyelitis model in marmoset monkeys, which are naturally infected with the EBV-related γ1-herpesvirus CalHV3. The data indicate that the infection of B cells with a γ1-herpesvirus endows them with the capacity to activate auto-aggressive CD8+ T cells specific for myelin oligodendrocyte glycoprotein.
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spelling pubmed-54661462017-06-12 An essential role of virus-infected B cells in the marmoset experimental autoimmune encephalomyelitis model ’t Hart, Bert A Kap, Yolanda S Mult Scler J Exp Transl Clin Review Infection with Epstein–Barr virus (EBV) has been associated with an enhanced risk of genetically susceptible individuals to develop multiple sclerosis (MS). However, an explanation for the contrast between the high EBV infection prevalence (60–90%) and the low MS prevalence (0.1%) eludes us. Here we propose a new concept for the EBV–MS association developed in the experimental autoimmune encephalomyelitis model in marmoset monkeys, which are naturally infected with the EBV-related γ1-herpesvirus CalHV3. The data indicate that the infection of B cells with a γ1-herpesvirus endows them with the capacity to activate auto-aggressive CD8+ T cells specific for myelin oligodendrocyte glycoprotein. SAGE Publications 2017-01-01 /pmc/articles/PMC5466146/ /pubmed/28607749 http://dx.doi.org/10.1177/2055217317690184 Text en © The Author(s) 2017 http://creativecommons.org/licenses/by-nc/3.0/ This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 3.0 License (http://www.creativecommons.org/licenses/by-nc/3.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).
spellingShingle Review
’t Hart, Bert A
Kap, Yolanda S
An essential role of virus-infected B cells in the marmoset experimental autoimmune encephalomyelitis model
title An essential role of virus-infected B cells in the marmoset experimental autoimmune encephalomyelitis model
title_full An essential role of virus-infected B cells in the marmoset experimental autoimmune encephalomyelitis model
title_fullStr An essential role of virus-infected B cells in the marmoset experimental autoimmune encephalomyelitis model
title_full_unstemmed An essential role of virus-infected B cells in the marmoset experimental autoimmune encephalomyelitis model
title_short An essential role of virus-infected B cells in the marmoset experimental autoimmune encephalomyelitis model
title_sort essential role of virus-infected b cells in the marmoset experimental autoimmune encephalomyelitis model
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5466146/
https://www.ncbi.nlm.nih.gov/pubmed/28607749
http://dx.doi.org/10.1177/2055217317690184
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