Abstract
The mechanism of action underlying the beneficial effect of IFNβ in Multiple Sclerosis is poorly understood. Experimental Autoimmune Encephalomyelitis (EAE) is the experimental model for Multiple Sclerosis; therefore, we investigated the effects of recombinant mouse IFNβ on the severity of EAE induced in SJL mice and on cytokine production by Th1 and Th2 lymphocytes. The results indicated that rmIFN β reduced the disease activity with an I.P. dosage of 10,000 U/day every other day, and successfully treated EAE mice revealed reduced amounts of IFN γ; no changes in the levels of IL4 were observed, although thera was a significant increase in IL10 and TGFβ production. Beneficial effects on EAE are associated with inhibition of inflammatory cytokines and stimulation of anti-inflammatory cytokines.