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Exp Neurol ; 221(1): 136-45, 2010 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-19879259

RESUMO

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 (MOG(35-55)) 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.


Assuntos
Transferência Adotiva/métodos , Linfócitos B/efeitos dos fármacos , Linfócitos B/fisiologia , Encefalomielite Autoimune Experimental/terapia , Imunossupressores/farmacologia , Peptídeos/farmacologia , Animais , Antígenos CD/metabolismo , Modelos Animais de Doenças , Encefalomielite Autoimune Experimental/induzido quimicamente , Encefalomielite Autoimune Experimental/imunologia , Citometria de Fluxo/métodos , Regulação da Expressão Gênica/fisiologia , Acetato de Glatiramer , Glicoproteínas , Interleucina-10/metabolismo , Interleucina-4/metabolismo , Ativação Linfocitária/efeitos dos fármacos , Ativação Linfocitária/imunologia , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Transgênicos , Proteínas da Mielina , Glicoproteína Associada a Mielina/genética , Glicoproteína Mielina-Oligodendrócito , Fragmentos de Peptídeos , Linfócitos T/efeitos dos fármacos , Linfócitos T/metabolismo , Fator de Crescimento Transformador beta/metabolismo
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