title: Mechanisms of modulation of experimental autoimmune encephalomyelitis by chronic Trichinella spiralis infection in Dark Agouti rats.
abstract: 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.
authors.affiliation: Institute for the Application of Nuclear Energy, University of Belgrade, Belgrade, Serbia. alisa@inep.co.rs
authors.forename: A
authors.initials: A
authors.lastname: Gruden-Movsesijan
authors.forename: N
authors.initials: N
authors.lastname: Ilic
authors.forename: M
authors.initials: M
authors.lastname: Mostarica-Stojkovic
authors.forename: S
authors.initials: S
authors.lastname: Stosic-Grujicic
authors.forename: M
authors.initials: M
authors.lastname: Milic
authors.forename: L
authors.initials: L
authors.lastname: Sofronic-Milosavljevic
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D015704:CD4 Antigens / Q000032:analysis; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000150:complications* / Q000276:immunology* / Q000473:pathology; D005260:Female; D051858:Forkhead Transcription Factors / Q000032:analysis; D007371:Interferon-gamma / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D020381:Interleukin-17 / Q000378:metabolism; D053645:Interleukin-2 Receptor alpha Subunit / Q000032:analysis; D015847:Interleukin-4 / Q000378:metabolism; D008198:Lymph Nodes / Q000276:immunology; D051381:Rats; D012720:Severity of Illness Index; D016176:T-Lymphocyte Subsets / Q000737:chemistry / Q000276:immunology; D017160:Trichinella spiralis / Q000276:immunology*; D014235:Trichinellosis / Q000150:complications* / Q000276:immunology* / Q000469:parasitology
chemical_list: D015704:CD4 Antigens; D051858:Forkhead Transcription Factors; C500522:Foxp3 protein, rat; D020381:Interleukin-17; D053645:Interleukin-2 Receptor alpha Subunit; D016753:Interleukin-10; D015847:Interleukin-4; D007371:Interferon-gamma