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CD4(+) T cells from multiple sclerosis patients respond to a commensal‐derived antigen

Multiple sclerosis, an immune‐mediated disease of the central nervous system, is characterized by the impaired function of regulatory cells that fail to suppress self‐reactive effector cells. We have previously found that polysaccharide A, a capsular antigen derived from the human gut commensal Bact...

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Autores principales: Burgess, Joseph N., Pant, Anudeep B., Kasper, Lloyd H., Colpitts Brass, Sara
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5682114/
https://www.ncbi.nlm.nih.gov/pubmed/29159195
http://dx.doi.org/10.1002/acn3.465
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author Burgess, Joseph N.
Pant, Anudeep B.
Kasper, Lloyd H.
Colpitts Brass, Sara
author_facet Burgess, Joseph N.
Pant, Anudeep B.
Kasper, Lloyd H.
Colpitts Brass, Sara
author_sort Burgess, Joseph N.
collection PubMed
description Multiple sclerosis, an immune‐mediated disease of the central nervous system, is characterized by the impaired function of regulatory cells that fail to suppress self‐reactive effector cells. We have previously found that polysaccharide A, a capsular antigen derived from the human gut commensal Bacteroides fragilis, can induce a population of regulatory T cells. Herein, we demonstrate that naïve T cells isolated from patients with multiple sclerosis have the capacity to acquire regulatory characteristics when stimulated in vitro with polysaccharide A. This study demonstrates the amplification of a regulatory T cell response by a gut‐derived commensal antigen in those with multiple sclerosis.
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spelling pubmed-56821142017-11-20 CD4(+) T cells from multiple sclerosis patients respond to a commensal‐derived antigen Burgess, Joseph N. Pant, Anudeep B. Kasper, Lloyd H. Colpitts Brass, Sara Ann Clin Transl Neurol Brief Communications Multiple sclerosis, an immune‐mediated disease of the central nervous system, is characterized by the impaired function of regulatory cells that fail to suppress self‐reactive effector cells. We have previously found that polysaccharide A, a capsular antigen derived from the human gut commensal Bacteroides fragilis, can induce a population of regulatory T cells. Herein, we demonstrate that naïve T cells isolated from patients with multiple sclerosis have the capacity to acquire regulatory characteristics when stimulated in vitro with polysaccharide A. This study demonstrates the amplification of a regulatory T cell response by a gut‐derived commensal antigen in those with multiple sclerosis. John Wiley and Sons Inc. 2017-09-27 /pmc/articles/PMC5682114/ /pubmed/29159195 http://dx.doi.org/10.1002/acn3.465 Text en © 2017 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals, Inc on behalf of American Neurological Association. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs (http://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Brief Communications
Burgess, Joseph N.
Pant, Anudeep B.
Kasper, Lloyd H.
Colpitts Brass, Sara
CD4(+) T cells from multiple sclerosis patients respond to a commensal‐derived antigen
title CD4(+) T cells from multiple sclerosis patients respond to a commensal‐derived antigen
title_full CD4(+) T cells from multiple sclerosis patients respond to a commensal‐derived antigen
title_fullStr CD4(+) T cells from multiple sclerosis patients respond to a commensal‐derived antigen
title_full_unstemmed CD4(+) T cells from multiple sclerosis patients respond to a commensal‐derived antigen
title_short CD4(+) T cells from multiple sclerosis patients respond to a commensal‐derived antigen
title_sort cd4(+) t cells from multiple sclerosis patients respond to a commensal‐derived antigen
topic Brief Communications
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5682114/
https://www.ncbi.nlm.nih.gov/pubmed/29159195
http://dx.doi.org/10.1002/acn3.465
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