Open AccessSuppression of experimental allergic encephalomyelitis by intraventricular administration of interferon‐gamma in Lewis rats
Author(s) -
VOORTHUIS J. A. C.,
UITDEHAAG B. M. J.,
GROOT C. J. A.,
GOEDE P. H.,
MEIDE P. H. VAN DER,
DIJKSTRA C. D.
Publication year - 1990
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1990.tb03315.x
Subject(s) - immunology , encephalomyelitis , medicine , interferon gamma , central nervous system , experimental autoimmune encephalomyelitis , autoimmune disease , pathogenesis , antigen , multiple sclerosis , immune system , antibody
SUMMARY 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.