Persistent inflammation in the CNS during chronic EAE despite local absence of IL-17 production

dc.contributor.authorZorzella-Pezavento, Sofia Fernanda Gonçalves [UNESP]
dc.contributor.authorChiuso-Minicucci, Fernanda [UNESP]
dc.contributor.authorFrança, Thais Graziela Donegá [UNESP]
dc.contributor.authorIshikawa, Larissa Lumi Watanabe [UNESP]
dc.contributor.authorDa Rosa, Larissa Camargo [UNESP]
dc.contributor.authorMarques, Camila
dc.contributor.authorIkoma, Maura Rosane Valerio
dc.contributor.authorSartori, Alexandrina [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionLaboratório de Citometria de Fluxo-Fundação
dc.date.accessioned2014-05-27T11:29:58Z
dc.date.available2014-05-27T11:29:58Z
dc.date.issued2013-07-19
dc.description.abstractExperimental autoimmune encephalomyelitis (EAE) is an artificially induced demyelination of the central nervous system (CNS) that resembles multiple sclerosis in its clinical, histopathological, and immunological features. Activated Th1 and Th17 cells are thought to be the main immunological players during EAE development. This study was designed to evaluate peripheral and local contribution of IL-17 to acute and chronic EAE stages. C57BL/6 mice were immunized with MOG plus complete Freund's adjuvant followed by pertussis toxin. Mice presented an initial acute phase characterized by accentuated weight loss and high clinical score, followed by a partial recovery when the animals reached normal body weight and smaller clinical scores. Spleen cells stimulated with MOG produced significantly higher levels of IFN-γ during the acute period whereas similar IL-17 levels were produced during both disease stages. CNS-infiltrating cells stimulated with MOG produced similar amounts of IFN-γ but, IL-17 was produced only at the acute phase of EAE. The percentage of Foxp3+ Treg cells, at the spleen and CNS, was elevated during both phases. The degree of inflammation was similar at both disease stages. Partial clinical recovery observed during chronic EAE was associated with no IL-17 production and presence of Foxp3+ Treg cells in the CNS. © 2013 Sofia Fernanda Gonçalves Zorzella-Pezavento et al.en
dc.description.affiliationDepartment of Microbiology and Immunology Biosciences Institute Universidade Estadual Paulista (UNESP), 18618-070 Botucatu, SP
dc.description.affiliationLaboratório de Citometria de Fluxo-Fundação, Dr. Amaral Carvalho, Jaú, SP
dc.description.affiliationUnespDepartment of Microbiology and Immunology Biosciences Institute Universidade Estadual Paulista (UNESP), 18618-070 Botucatu, SP
dc.identifierhttp://dx.doi.org/10.1155/2013/519627
dc.identifier.citationMediators of Inflammation, v. 2013.
dc.identifier.doi10.1155/2013/519627
dc.identifier.file2-s2.0-84880150391.pdf
dc.identifier.issn0962-9351
dc.identifier.issn1466-1861
dc.identifier.lattes4977572416129527
dc.identifier.scopus2-s2.0-84880150391
dc.identifier.urihttp://hdl.handle.net/11449/76011
dc.identifier.wosWOS:000321660200001
dc.language.isoeng
dc.relation.ispartofMediators of Inflammation
dc.relation.ispartofjcr3.549
dc.relation.ispartofsjr1,370
dc.relation.ispartofsjr1,370
dc.rights.accessRightsAcesso aberto
dc.sourceScopus
dc.subjectFreund adjuvant
dc.subjectgamma interferon
dc.subjectinterleukin 17
dc.subjectmyelin oligodendrocyte glycoprotein
dc.subjectpertussis toxin
dc.subjecttranscription factor FOXP3
dc.subjectallergic encephalomyelitis
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectbody weight
dc.subjectcell infiltration
dc.subjectcontrolled study
dc.subjectcytokine production
dc.subjectdisease severity
dc.subjectfemale
dc.subjectinflammatory infiltrate
dc.subjectmouse
dc.subjectnervous system inflammation
dc.subjectnonhuman
dc.subjectpriority journal
dc.subjectregulatory T lymphocyte
dc.subjectscoring system
dc.subjectspleen cell
dc.subjectweight reduction
dc.titlePersistent inflammation in the CNS during chronic EAE despite local absence of IL-17 productionen
dc.typeArtigo
dcterms.licensehttp://www.hindawi.com/journals/aaa/guidelines/
unesp.author.lattes4977572416129527[8]
unesp.author.orcid0000-0003-4557-3331[8]
unesp.campusUniversidade Estadual Paulista (Unesp), Instituto de Biociências, Botucatupt
unesp.departmentMicrobiologia e Imunologia - IBBpt

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