| First Author | Kahl KG | Year | 2004 |
| Journal | Neurosci Lett | Volume | 358 |
| Issue | 1 | Pages | 58-62 |
| PubMed ID | 15016434 | Mgi Jnum | J:88809 |
| Mgi Id | MGI:3037224 | Doi | 10.1016/j.neulet.2003.12.095 |
| Citation | Kahl KG, et al. (2004) Experimental autoimmune encephalomyelitis in mice with a targeted deletion of the inducible nitric oxide synthase gene: increased T-helper 1 response. Neurosci Lett 358(1):58-62 |
| abstractText | 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. |
