Suppression of experimental allergic encephalomyelitis by intraventricular administration of interferon-gamma in Lewis rats


Christine D. Dijkstra, Department of Cell Biology, Medical Faculty, Vrije Universiteit, P.O. Box 7161, 1007 MC Amsterdam, The Netherlands.


Experimental allergic encephalomyelitis (EAE) is an autoimmune inflammatory disease of the central nervous system (CNS) which causes paralysis. Several studies have reported the involvement of Ia antigen-expressing cells in the pathogenesis of EAE. Interferon-gamma (IFN-γ) can induce Ia antigen expression on a wide range of cells. We examined the effect of IFN-γ on EAE in Lewis rats. Systemically administered IFN-γ did not change the disease course of EAE, whereas IFN-γ applied locally into the ventricular system of the CNS resulted in complete suppression of clinical signs. Furthermore, we found that systemic administration of anti-IFN-γ just prior to the onset of clinical symptoms resulted in a more severe disease course. We conclude that IFN-γ is capable of exerting a suppressive action in EAE, possibly through induction of Ia antigen expression or through the induction of suppressive mechanisms locally in the CNS.