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Myelin oligodendrocyte glycoprotein has a dual role in T cell autoimmunity against central nervous system myelin

BACKGROUND: Myelin oligodendrocyte glycoprotein (MOG) is a candidate primary target of the autoimmune attack on the central nervous system (CNS) in multiple sclerosis (MS). However, the physiological function of MOG has been unclear for a long time. OBJECTIVE: We propose that MOG has a central role...

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Autores principales: ’t Hart, Bert A, Weissert, Robert
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5433322/
https://www.ncbi.nlm.nih.gov/pubmed/28607715
http://dx.doi.org/10.1177/2055217316630999
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author ’t Hart, Bert A
Weissert, Robert
author_facet ’t Hart, Bert A
Weissert, Robert
author_sort ’t Hart, Bert A
collection PubMed
description BACKGROUND: Myelin oligodendrocyte glycoprotein (MOG) is a candidate primary target of the autoimmune attack on the central nervous system (CNS) in multiple sclerosis (MS). However, the physiological function of MOG has been unclear for a long time. OBJECTIVE: We propose that MOG has a central role in the regulation of tolerance and autoimmunity. CONCLUSION: The interaction of MOG with DC-SIGN, an innate antigen receptor of myeloid antigen-presenting cells (m-APCs), present inside the CNS (microglia) or in draining lymph nodes (dendritic cells; DCs), keeps these cells in an immature/tolerogenic state. We postulate that this tolerogenic mechanism may be disturbed in MS by unknown factors.
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spelling pubmed-54333222017-06-12 Myelin oligodendrocyte glycoprotein has a dual role in T cell autoimmunity against central nervous system myelin ’t Hart, Bert A Weissert, Robert Mult Scler J Exp Transl Clin Review BACKGROUND: Myelin oligodendrocyte glycoprotein (MOG) is a candidate primary target of the autoimmune attack on the central nervous system (CNS) in multiple sclerosis (MS). However, the physiological function of MOG has been unclear for a long time. OBJECTIVE: We propose that MOG has a central role in the regulation of tolerance and autoimmunity. CONCLUSION: The interaction of MOG with DC-SIGN, an innate antigen receptor of myeloid antigen-presenting cells (m-APCs), present inside the CNS (microglia) or in draining lymph nodes (dendritic cells; DCs), keeps these cells in an immature/tolerogenic state. We postulate that this tolerogenic mechanism may be disturbed in MS by unknown factors. SAGE Publications 2016-02-07 /pmc/articles/PMC5433322/ /pubmed/28607715 http://dx.doi.org/10.1177/2055217316630999 Text en © The Author(s) 2016 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 page(https://us.sagepub.com/en-us/nam/open-access-at-sage).
spellingShingle Review
’t Hart, Bert A
Weissert, Robert
Myelin oligodendrocyte glycoprotein has a dual role in T cell autoimmunity against central nervous system myelin
title Myelin oligodendrocyte glycoprotein has a dual role in T cell autoimmunity against central nervous system myelin
title_full Myelin oligodendrocyte glycoprotein has a dual role in T cell autoimmunity against central nervous system myelin
title_fullStr Myelin oligodendrocyte glycoprotein has a dual role in T cell autoimmunity against central nervous system myelin
title_full_unstemmed Myelin oligodendrocyte glycoprotein has a dual role in T cell autoimmunity against central nervous system myelin
title_short Myelin oligodendrocyte glycoprotein has a dual role in T cell autoimmunity against central nervous system myelin
title_sort myelin oligodendrocyte glycoprotein has a dual role in t cell autoimmunity against central nervous system myelin
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5433322/
https://www.ncbi.nlm.nih.gov/pubmed/28607715
http://dx.doi.org/10.1177/2055217316630999
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