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• W2019952244 abstract "Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) thought to be primarily mediated by T cells. However, emerging evidence supports an important role for B cells in the pathogenesis and inhibition of MS. Glatiramer acetate (GA), a Food and Drug Administration-approved drug for the treatment of MS, has a good safety profile. But GA's mechanism of action in MS is still elusive. In this study, we showed that B cells from GA-treated mice increased production of IL-10 and reduced expression of co-stimulatory molecules viz.: CD80 and CD86. B cells from GA-treated mice also diminished proliferation of myelin oligodendrocyte glycoprotein (MOG35-55) specific T cells. Purified B cells transferred from GA-treated mice suppressed experimental autoimmune encephalomyelitis (EAE) in recipient mice compared with B cells transferred from mice treated with PBS or ovalbumin. The treatment effect of GA in EAE was abrogated in B cell-deficient mice. Transfer of B cells from GA-treated mice inhibited the proliferation of autoreactive T cells as well as the development of Th1 and Th17 cells but promoted IL-10 production in recipient mice. The number of peripheral CD11b+ macrophages in recipient mice also decreased after transfer of B cells from GA-treated mice; however, the number of dendritic cells and regulatory T cells remained unaltered. These results suggest that B cells are important to the protective effects of GA in EAE." @default.
• W2019952244 created "2016-06-24" @default.
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• W2019952244 date "2010-01-01" @default.
• W2019952244 modified "2023-09-26" @default.
• W2019952244 title "B cells from glatiramer acetate-treated mice suppress experimental autoimmune encephalomyelitis" @default.
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• W2019952244 doi "https://doi.org/10.1016/j.expneurol.2009.10.015" @default.
• W2019952244 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19879259" @default.
• W2019952244 hasPublicationYear "2010" @default.
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