title: Experimental autoimmune encephalomyelitis in mice with a targeted deletion of the inducible nitric oxide synthase gene: increased T-helper 1 response.
abstract: Mice with a targeted deletion of the cytokine-inducible nitric oxide synthase gene (iNOS(-/-)) show increased severity of experimental autoimmune encephalomyelitis (EAE). We studied the mechanisms of susceptibility to myelin-basic protein-induced 'active' EAE in iNOS(-/-) mice. Spleen cells and lymph node cells from iNOS(-/-) mice with EAE showed a significantly enhanced ex vivo proliferation and production of T-helper 1 (Th1) cytokines (interferon-gamma by 157 and 57% and tumor-necrosis-factor-alpha by 86 and 27%, respectively). We conclude that NO produced by iNOS plays a protective role in EAE probably by inhibiting the production of Th1 cytokines and T cell proliferation.
authors.affiliation: Department of Neurology, Julius-Maximilians-University, Josef-Schneider Str. 11, D-97080 Würzburg, Germany.
authors.forename: Kai G
authors.initials: KG
authors.lastname: Kahl
authors.forename: Harald H H W
authors.initials: HH
authors.lastname: Schmidt
authors.forename: Stefan
authors.initials: S
authors.lastname: Jung
authors.forename: Paula
authors.initials: P
authors.lastname: Sherman
authors.forename: Klaus V
authors.initials: KV
authors.lastname: Toyka
authors.forename: Jürgen
authors.initials: J
authors.lastname: Zielasek
mesh_terms: D000818:Animals; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000201:enzymology* / Q000235:genetics* / Q000276:immunology; D017353:Gene Deletion; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D019001:Nitric Oxide Synthase / Q000096:biosynthesis / Q000172:deficiency* / Q000235:genetics; D052247:Nitric Oxide Synthase Type II; D018417:Th1 Cells / Q000201:enzymology* / Q000276:immunology
chemical_list: D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse