Immunopathogenesis of multiple sclerosis

Multiple sclerosis (MS) is a suspected autoimmune disease in which myelin-specific CD4+ and CD8+ T cells enter the central nervous system (CNS) and initiate an inflammatory response directed against myelin and other components of the CNS. Acute MS exacerbations are believed be...

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Main Author: Racke Michael
Format: Article
Language:English
Published: Wolters Kluwer Medknow Publications 2009-01-01
Series:Annals of Indian Academy of Neurology
Subjects:
Online Access:http://www.annalsofian.org/article.asp?issn=0972-2327;year=2009;volume=12;issue=4;spage=215;epage=220;aulast=Racke
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spelling doaj-6ba5f672760a4963ab05953426f19b0c2020-11-24T22:17:13ZengWolters Kluwer Medknow PublicationsAnnals of Indian Academy of Neurology0972-23271998-35492009-01-01124215220Immunopathogenesis of multiple sclerosisRacke MichaelMultiple sclerosis (MS) is a suspected autoimmune disease in which myelin-specific CD4+ and CD8+ T cells enter the central nervous system (CNS) and initiate an inflammatory response directed against myelin and other components of the CNS. Acute MS exacerbations are believed be the result of active inflammation, and progression of disability is generally believed to reflect accumulation of damage to the CNS, particularly axonal damage. Over the last several years, the pathophysiology of MS is being appreciated to be much more complex, and it appears that the development of the MS plaque involves a large number of cell populations, including CD8+ T lymphocytes, B cells, and Th17 cells (a population of helper T cells that secrete the inflammatory cytokine IL-17). The axonal transection and degeneration that is thought to represent the basis for progressive MS is now recognized to begin early in the disease process and to continue in the progressive forms of the disease. Molecules important for limiting aberrant neural connections in the CNS have been identified, which suppress axonal sprouting and regeneration of transected axons within the CNS. Pathways have also been identified that prevent remyelination of the MS lesion by oligodendrocyte precursors. Novel neuroimaging methodologies and potential biomarkers are being developed to monitor various aspects of the disease process in MS. As we identify the pathways responsible for the clinical phenomena of MS, we will be able to develop new therapeutic strategies for this disabling illness of young adults.http://www.annalsofian.org/article.asp?issn=0972-2327;year=2009;volume=12;issue=4;spage=215;epage=220;aulast=RackeMagnetic resonance imagingmultiple sclerosispathogenesisreview
collection DOAJ
language English
format Article
sources DOAJ
author Racke Michael
spellingShingle Racke Michael
Immunopathogenesis of multiple sclerosis
Annals of Indian Academy of Neurology
Magnetic resonance imaging
multiple sclerosis
pathogenesis
review
author_facet Racke Michael
author_sort Racke Michael
title Immunopathogenesis of multiple sclerosis
title_short Immunopathogenesis of multiple sclerosis
title_full Immunopathogenesis of multiple sclerosis
title_fullStr Immunopathogenesis of multiple sclerosis
title_full_unstemmed Immunopathogenesis of multiple sclerosis
title_sort immunopathogenesis of multiple sclerosis
publisher Wolters Kluwer Medknow Publications
series Annals of Indian Academy of Neurology
issn 0972-2327
1998-3549
publishDate 2009-01-01
description Multiple sclerosis (MS) is a suspected autoimmune disease in which myelin-specific CD4+ and CD8+ T cells enter the central nervous system (CNS) and initiate an inflammatory response directed against myelin and other components of the CNS. Acute MS exacerbations are believed be the result of active inflammation, and progression of disability is generally believed to reflect accumulation of damage to the CNS, particularly axonal damage. Over the last several years, the pathophysiology of MS is being appreciated to be much more complex, and it appears that the development of the MS plaque involves a large number of cell populations, including CD8+ T lymphocytes, B cells, and Th17 cells (a population of helper T cells that secrete the inflammatory cytokine IL-17). The axonal transection and degeneration that is thought to represent the basis for progressive MS is now recognized to begin early in the disease process and to continue in the progressive forms of the disease. Molecules important for limiting aberrant neural connections in the CNS have been identified, which suppress axonal sprouting and regeneration of transected axons within the CNS. Pathways have also been identified that prevent remyelination of the MS lesion by oligodendrocyte precursors. Novel neuroimaging methodologies and potential biomarkers are being developed to monitor various aspects of the disease process in MS. As we identify the pathways responsible for the clinical phenomena of MS, we will be able to develop new therapeutic strategies for this disabling illness of young adults.
topic Magnetic resonance imaging
multiple sclerosis
pathogenesis
review
url http://www.annalsofian.org/article.asp?issn=0972-2327;year=2009;volume=12;issue=4;spage=215;epage=220;aulast=Racke
work_keys_str_mv AT rackemichael immunopathogenesisofmultiplesclerosis
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