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

• Published in: Clinical and experimental immunology Vol. 81; no. 2; pp. 183 - 188
• Main Authors: VOORTHUIS, J. A. C., UITDEHAAG, B. M. J., GROOT, C. J. A., GOEDE, P. H., MEIDE, P. H. VAN DER, DIJKSTRA, C. D.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.08.1990; Blackwell
• Subjects: Animals; Antibodies, Monoclonal - administration & dosage; Antibodies, Monoclonal - therapeutic use; Autoimmunity (experimental aspects and models); Biological and medical sciences; Cerebellum - immunology; Cerebellum - pathology; Encephalomyelitis, Autoimmune, Experimental - pathology; Encephalomyelitis, Autoimmune, Experimental - prevention & control; Encephalomyelitis, Autoimmune, Experimental - therapy; experimental allergic encephalomyelitis; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Histocompatibility Antigens Class II - biosynthesis; Ia antigen expression; Immunoenzyme Techniques; Injections, Intraperitoneal; Injections, Intraventricular; Interferon-gamma - administration & dosage; Interferon-gamma - immunology; Interferon-gamma - therapeutic use; interferon‐gamma; Male; Optic Nerve - immunology; Optic Nerve - pathology; Rats; Rats, Inbred Lew; Recombinant Proteins; suppression rat; Allergy; Nervous system diseases; Encephalomyelitis; Rat; Suppression; Rodentia; Class II histocompatibility antigen; Cytokine; Autoimmune disease; Histology; Biological activity; Vertebrata; Experimental disease; Mammalia; Gamma interferon
• ISSN: 0009-9104; 1365-2249
• DOI: 10.1111/j.1365-2249.1990.tb03315.x

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.