Cargando…

Autoreactive lymphocytes in multiple sclerosis: Pathogenesis and treatment target

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) characterized by destruction of the myelin sheath structure. The loss of myelin leads to damage of a neuron’s axon and cell body, which is identified as brain lesions on magnetic resonance image (MRI). The...

Descripción completa

Detalles Bibliográficos
Autores principales: Liu, Rongzeng, Du, Shushu, Zhao, Lili, Jain, Sahil, Sahay, Kritika, Rizvanov, Albert, Lezhnyova, Vera, Khaibullin, Timur, Martynova, Ekaterina, Khaiboullina, Svetlana, Baranwal, Manoj
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9539795/
https://www.ncbi.nlm.nih.gov/pubmed/36211343
http://dx.doi.org/10.3389/fimmu.2022.996469
_version_ 1784803568240295936
author Liu, Rongzeng
Du, Shushu
Zhao, Lili
Jain, Sahil
Sahay, Kritika
Rizvanov, Albert
Lezhnyova, Vera
Khaibullin, Timur
Martynova, Ekaterina
Khaiboullina, Svetlana
Baranwal, Manoj
author_facet Liu, Rongzeng
Du, Shushu
Zhao, Lili
Jain, Sahil
Sahay, Kritika
Rizvanov, Albert
Lezhnyova, Vera
Khaibullin, Timur
Martynova, Ekaterina
Khaiboullina, Svetlana
Baranwal, Manoj
author_sort Liu, Rongzeng
collection PubMed
description Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) characterized by destruction of the myelin sheath structure. The loss of myelin leads to damage of a neuron’s axon and cell body, which is identified as brain lesions on magnetic resonance image (MRI). The pathogenesis of MS remains largely unknown. However, immune mechanisms, especially those linked to the aberrant lymphocyte activity, are mainly responsible for neuronal damage. Th1 and Th17 populations of lymphocytes were primarily associated with MS pathogenesis. These lymphocytes are essential for differentiation of encephalitogenic CD8(+) T cell and Th17 lymphocyte crossing the blood brain barrier and targeting myelin sheath in the CNS. B-lymphocytes could also contribute to MS pathogenesis by producing anti-myelin basic protein antibodies. In later studies, aberrant function of Treg and Th9 cells was identified as contributing to MS. This review summarizes the aberrant function and count of lymphocyte, and the contributions of these cell to the mechanisms of MS. Additionally, we have outlined the novel MS therapeutics aimed to amend the aberrant function or counts of these lymphocytes.
format Online
Article
Text
id pubmed-9539795
institution National Center for Biotechnology Information
language English
publishDate 2022
publisher Frontiers Media S.A.
record_format MEDLINE/PubMed
spelling pubmed-95397952022-10-08 Autoreactive lymphocytes in multiple sclerosis: Pathogenesis and treatment target Liu, Rongzeng Du, Shushu Zhao, Lili Jain, Sahil Sahay, Kritika Rizvanov, Albert Lezhnyova, Vera Khaibullin, Timur Martynova, Ekaterina Khaiboullina, Svetlana Baranwal, Manoj Front Immunol Immunology Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) characterized by destruction of the myelin sheath structure. The loss of myelin leads to damage of a neuron’s axon and cell body, which is identified as brain lesions on magnetic resonance image (MRI). The pathogenesis of MS remains largely unknown. However, immune mechanisms, especially those linked to the aberrant lymphocyte activity, are mainly responsible for neuronal damage. Th1 and Th17 populations of lymphocytes were primarily associated with MS pathogenesis. These lymphocytes are essential for differentiation of encephalitogenic CD8(+) T cell and Th17 lymphocyte crossing the blood brain barrier and targeting myelin sheath in the CNS. B-lymphocytes could also contribute to MS pathogenesis by producing anti-myelin basic protein antibodies. In later studies, aberrant function of Treg and Th9 cells was identified as contributing to MS. This review summarizes the aberrant function and count of lymphocyte, and the contributions of these cell to the mechanisms of MS. Additionally, we have outlined the novel MS therapeutics aimed to amend the aberrant function or counts of these lymphocytes. Frontiers Media S.A. 2022-09-23 /pmc/articles/PMC9539795/ /pubmed/36211343 http://dx.doi.org/10.3389/fimmu.2022.996469 Text en Copyright © 2022 Liu, Du, Zhao, Jain, Sahay, Rizvanov, Lezhnyova, Khaibullin, Martynova, Khaiboullina and Baranwal https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Liu, Rongzeng
Du, Shushu
Zhao, Lili
Jain, Sahil
Sahay, Kritika
Rizvanov, Albert
Lezhnyova, Vera
Khaibullin, Timur
Martynova, Ekaterina
Khaiboullina, Svetlana
Baranwal, Manoj
Autoreactive lymphocytes in multiple sclerosis: Pathogenesis and treatment target
title Autoreactive lymphocytes in multiple sclerosis: Pathogenesis and treatment target
title_full Autoreactive lymphocytes in multiple sclerosis: Pathogenesis and treatment target
title_fullStr Autoreactive lymphocytes in multiple sclerosis: Pathogenesis and treatment target
title_full_unstemmed Autoreactive lymphocytes in multiple sclerosis: Pathogenesis and treatment target
title_short Autoreactive lymphocytes in multiple sclerosis: Pathogenesis and treatment target
title_sort autoreactive lymphocytes in multiple sclerosis: pathogenesis and treatment target
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9539795/
https://www.ncbi.nlm.nih.gov/pubmed/36211343
http://dx.doi.org/10.3389/fimmu.2022.996469
work_keys_str_mv AT liurongzeng autoreactivelymphocytesinmultiplesclerosispathogenesisandtreatmenttarget
AT dushushu autoreactivelymphocytesinmultiplesclerosispathogenesisandtreatmenttarget
AT zhaolili autoreactivelymphocytesinmultiplesclerosispathogenesisandtreatmenttarget
AT jainsahil autoreactivelymphocytesinmultiplesclerosispathogenesisandtreatmenttarget
AT sahaykritika autoreactivelymphocytesinmultiplesclerosispathogenesisandtreatmenttarget
AT rizvanovalbert autoreactivelymphocytesinmultiplesclerosispathogenesisandtreatmenttarget
AT lezhnyovavera autoreactivelymphocytesinmultiplesclerosispathogenesisandtreatmenttarget
AT khaibullintimur autoreactivelymphocytesinmultiplesclerosispathogenesisandtreatmenttarget
AT martynovaekaterina autoreactivelymphocytesinmultiplesclerosispathogenesisandtreatmenttarget
AT khaiboullinasvetlana autoreactivelymphocytesinmultiplesclerosispathogenesisandtreatmenttarget
AT baranwalmanoj autoreactivelymphocytesinmultiplesclerosispathogenesisandtreatmenttarget