Different MOG(35-55) concentrations induce distinguishable inflammation through early regulatory response by IL-10 and TGF-beta in mice CNS despite unchanged clinical course

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dc.contributor.author Dias, Alyria Teixeira
dc.contributor.author Ribeiro De Castro, Sandra Bertelli
dc.contributor.author De Souza Alves, Caio Cesar
dc.contributor.author Mesquita, Felipe Pereira
dc.contributor.author Visona De Figueiredo, Nathalia Stela
dc.contributor.author Evangelista, Marcilene Gomes
dc.contributor.author Marques Nogueira Castanon, Maria Christina
dc.contributor.author Juliano, Maria Aparecida [UNIFESP]
dc.contributor.author Ferreira, Ana Paula
dc.date.accessioned 2016-01-24T14:39:58Z
dc.date.available 2016-01-24T14:39:58Z
dc.date.issued 2015-02-01
dc.identifier http://dx.doi.org/10.1016/j.cellimm.2014.12.009
dc.identifier.citation Cellular Immunology. San Diego: Academic Press Inc Elsevier Science, v. 293, n. 2, p. 87-94, 2015.
dc.identifier.issn 0008-8749
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/38688
dc.description.abstract Multiple sclerosis (MS) shows distinct clinical courses. Experimental autoimmune encephalomyelitis (EAE), a model to study multiple sclerosis, can be induced by different protocols, which show distinct cytokine and antibody production. the factors involved in this heterogeneity remain unclear. the relevance of MUG concentration in triggering a regulatory response in the chronic model of EAE is imprecise. the aim of this study was investigate if 100 or 300 mu g of MOG(35-55) could induce different EAE profiles. Modifications in the concentration of MUG were able to change the patterns of chemokines, cytokines, percentage of cells, inflammatory infiltrate and the development of a regulatory response. However, these changes were unable to modify the intensity of response, which explains the chronic progression of the disease in both concentrations. the results presented in this study contribute to understanding the intricate mechanisms that trigger EAE and provide insights into the pathogenesis of various forms of MS. (C) 2015 Elsevier Inc. All rights reserved. en
dc.description.sponsorship Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorship Fundação de Amparo à Pesquisa do Estado de Minas Gerais (FAPEMIG)
dc.description.sponsorship Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.format.extent 87-94
dc.language.iso eng
dc.publisher Elsevier B.V.
dc.relation.ispartof Cellular Immunology
dc.rights Acesso restrito
dc.subject Multiple sclerosis en
dc.subject Animal model en
dc.subject Autoimmunity en
dc.subject MOG(35-55) en
dc.subject Cytokines en
dc.title Different MOG(35-55) concentrations induce distinguishable inflammation through early regulatory response by IL-10 and TGF-beta in mice CNS despite unchanged clinical course en
dc.type Artigo
dc.rights.license http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.contributor.institution Univ Fed Juiz de Fora
dc.contributor.institution Fed Univ Valleys Jequitinhonha & Mucuri
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliation Univ Fed Juiz de Fora, Inst Biol Sci, IMUNOCET, Dept Parasitol Microbiol & Immunol, BR-36036900 Juiz de Fora, MG, Brazil
dc.description.affiliation Univ Fed Juiz de Fora, Dept Pharm, Governador Valadares, Brazil
dc.description.affiliation Fed Univ Valleys Jequitinhonha & Mucuri, Fac Med, Teofilo Otoni, Brazil
dc.description.affiliation Univ Fed Juiz de Fora, Dept Morphol, BR-36036900 Juiz de Fora, MG, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Dept Biophys, São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Biophys, São Paulo, Brazil
dc.description.sponsorshipID CNPq: 481459/2009-0
dc.description.sponsorshipID CNPq: 303369/2009-4
dc.description.sponsorshipID CNPq: 306575/2012-4
dc.description.sponsorshipID CNPq: 470768/2013-4
dc.description.sponsorshipID FAPEMIG: 02236/10
dc.description.sponsorshipID FAPEMIG: PPM 0216/10
dc.description.sponsorshipID FAPEMIG: 00269-14
dc.description.sponsorshipID CAPES: PNPD-2882/2011
dc.identifier.doi 10.1016/j.cellimm.2014.12.009
dc.description.source Web of Science
dc.identifier.wos WOS:000350089900005



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