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dc.creatorStošić-Grujičić, Stanislava
dc.creatorGruden-Movsesijan, Alisa
dc.creatorRadulović, Nataša
dc.creatorMostarica-Stojković, Marija B
dc.creatorMilić, M
dc.creatorSofronić-Milosavljević, Ljiljana
dc.date.accessioned2017-11-23T11:10:48Z
dc.date.available2015-11-17T10:26:51Z
dc.date.issued2010sr
dc.identifier.issn0141-9838sr
dc.identifier.otherRad_konverzija_3368sr
dc.identifier.urihttps://radar.ibiss.bg.ac.rs/handle/123456789/1373
dc.description.abstractP>Trichinella spiralis is a helminth that provokes Th2 and anti-inflammatory type responses in an infected host. Our previous studies using Dark Agouti (DA) rats indicated that T. spiralis infection reduced experimental autoimmune encephalomyelitis (EAE) severity in rats. The aim of this study was to analyse the mechanisms underlying EAE suppression driven by T. spiralis infection. Reduced clinical and histological manifestations of the disease were accompanied by increased IL-4 and IL-10 production and decreased IFN-gamma and IL-17 production in draining lymph node cells. This indicates that T. spiralis infection successfully maintains a Th2 cytokine bias regardless of EAE induction. High IL-10 signifies parasite-induced anti-inflammatory and/or regulatory cell responses. Transfer of splenic T cell-enriched population of cells from T. spiralis-infected rats into EAE immunized rats caused amelioration of EAE and in some cases protection from disease development. This population of cells contained higher proportion of CD4+ CD25+ Foxp3+ regulatory cells and produced high level of IL-10 when compared with uninfected rats.en
dc.description.sponsorshipMinistry of Science and Technological Development of the Republic of Serbia [143047, 143029, 145066]sr
dc.language.isoEnglishsr
dc.rightsrestrictedAccess
dc.sourceParasite Immunologysr
dc.titleMechanisms of modulation of experimental autoimmune encephalomyelitis by chronic Trichinella spiralis infection in Dark Agouti ratsen
dc.typearticle
dc.rights.licenseARR
dcterms.abstractИлић, Натаса В; Стошић-Грујичић, Станислава Д.; Софронић-Милосављевић, Љиљана; Груден-Мовсесијан, Aлиса; Мостарица-Стојковић, Марија Б; Милић, М;
dc.citation.issue6sr
dc.citation.volume32sr
dc.citation.epage459sr
dc.type.versionpublishedVersionen
dc.citation.rankM21
dc.identifier.rcubhttps://hdl.handle.net/21.15107/rcub_ibiss_1373


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