Experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis, is an autoimmune disorder seen in mice and rats following immunization with myelin basic protein (MBP) or MBP-derived peptides. IFN-γ, a cytokine produced by a variety of cells, is involved in many inflammatory and immune regulatory events. Contradictory results concerning exacerbations and the disease course were seen comparing injections of IFN-γ in humans suffering from multiple sclerosis to studies using anti-IFN-γ Abs in mice with EAE. To study the role of IFN-γ and IFN-γ-producing cells in EAE, we crossed IFN-γ knockout mice (H-2b) (unable to produce IFN-γ due to the disruption of the IFN-γ gene) with an EAE-susceptible mouse strain, B10.PL (H-2u). EAE was seen in IFN-γ knockout mice, heterozygotic (IFN-γ +/-) mice, as well as wild-type littermates following immunization with MBP. Histologic analyses of the central nervous system of IFN-γ knockout mice with EAE revealed massive infiltrates composed of lymphocytes, macrophages, and granulocytes. We conclude that the presence of IFN-γ is not crucial to the induction or the clinical course of EAE.
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Ferber et al. (1996) studied this question.