J Neuroimmunol. 2003 Dec;145(1-2):86-90
van der Veen RC, Dietlin TA, Hofman FM.
Department of Neurology, University of Southern California, Keck School of Medicine, MCA 245, 1333 San Pablo Street, 90033, Los Angeles, CA, USA
The cause of increased severity of experimental allergic encephalomyelitis (EAE) in inducible nitric oxide synthase (iNOS)(-/-) or IFN-gamma(-/-) mice remains unclear.
Transient chimeras were generated to examine the source of iNOS-inducing IFN-gamma in the central nervous system (CNS).
IFNgamma(-/-) donor cells induced severe EAE but no iNOS expression in the CNS of wild-type recipients upon their immunization.
By contrast, milder EAE, but strong iNOS expression was induced in immunized recipients of wild-type donor spleen cells.
These results demonstrate that IFN-gamma secretion by infiltrating spleen cells is essential for iNOS expression during CNS inflammation.
Furthermore, splenic NO is immunosuppressive.