Abstract
IL-18 deficient (IL-18 −/−) mice were used to investigate the role of IL-18 in the pathogenesis of experimental autoimmune neuritis (EAN) which was induced by immunization of the mice with P0 protein peptide 180–199. The clinical course was not different between IL-18 −/− and wild-type mice. The splenic mononuclear cell (MNC) proliferation was also similar in both animal groups. However, the percentages of IFN-γ, IL-10 and IL-12 positive cells were decreased among infiltrating MNC of cauda equine in IL-18 −/− mice. This indicates that IL-18 deficiency inhibits the production of both Th1 and Th2 cytokines in the target organ of mice with EAN.
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