Neurosci Lett. 2004 Mar 18;358(1):58-62
Kahl KG, Schmidt HH, Jung S, Sherman P, Toyka KV, Zielasek J.
Department of Neurology, Julius-Maximilians-University, Josef-Schneider Str. 11, D-97080 Wurzburg, Germany.
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.