T cells in multiple sclerosis and experimental autoimmune encephalomyelitis.
AffiliationImmune Regulation Research Group, School of Biochemistry and Immunology, Trinity , College, St Vincent's University Hospital, Dublin, Ireland.
Encephalomyelitis, Autoimmune, Experimental/*immunology/pathology
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CitationClin Exp Immunol. 2010 Oct;162(1):1-11. doi: 10.1111/j.1365-2249.2010.04143.x.
JournalClinical and experimental immunology
AbstractMultiple sclerosis (MS) is a demyelinating inflammatory disorder of the central nervous system (CNS), which involves autoimmune responses to myelin antigens. Studies in experimental autoimmune encephalomyelitis (EAE), an animal model for MS, have provided convincing evidence that T cells specific for self-antigens mediate pathology in these diseases. Until recently, T helper type 1 (Th1) cells were thought to be the main effector T cells responsible for the autoimmune inflammation. However more recent studies have highlighted an important pathogenic role for CD4(+) T cells that secrete interleukin (IL)-17, termed Th17, but also IL-17-secreting gammadelta T cells in EAE as well as other autoimmune and chronic inflammatory conditions. This has prompted intensive study of the induction, function and regulation of IL-17-producing T cells in MS and EAE. In this paper, we review the contribution of Th1, Th17, gammadelta, CD8(+) and regulatory T cells as well as the possible development of new therapeutic approaches for MS based on manipulating these T cell subtypes.
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