期刊
NEUROSCIENCE LETTERS
卷 358, 期 1, 页码 58-62出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2003.12.095
关键词
inducible nitric oxide synthase knockout mice; multiple sclerosis; T-helper 1/T-helper 2 immune response; oxidative stress; peroxynitrite
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. (C) 2003 Elsevier Ireland Ltd. All rights reserved.
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