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

J. A. C. Voorthuis, Bernard M.J. Uitdehaag(University of Amsterdam), Corline J.A. De Groot, Peter H Goede(University of Amsterdam), Peter H. van der Meide(Biomedical Primate Research Centre), C.D. Dijkstra
Clinical & Experimental Immunology
August 1, 1990
Cited by 217Open Access
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Abstract

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-gamma) can induce Ia antigen expression on a wide range of cells. We examined the effect of IFN-gamma on EAE in Lewis rats. Systemically administered IFN-gamma did not change the disease course of EAE, whereas IFN-gamma 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-gamma just prior to the onset of clinical symptoms resulted in a more severe disease course. We conclude that IFN-gamma 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.


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