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Title: Experimental autoimmune encephalomyelitis in mice with a targeted deletion of the inducible nitric oxide synthase gene: increased T-helper 1 response. Author: Kahl KG, Schmidt HH, Jung S, Sherman P, Toyka KV, Zielasek J. Journal: Neurosci Lett; 2004 Mar 18; 358(1):58-62. PubMed ID: 15016434. 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.[Abstract] [Full Text] [Related] [New Search]