Induction of low dose oral tolerance in IL-10 deficient mice with experimental autoimmune encephalomyelitis

IL-10 has been shown to be an important anti-inflammatory mediator that has both down-regulatory and immunomodulatory effects. Utilizing IL-10 −/− mice we demonstrate the induction of low dose oral tolerance characterized by the up-regulation of TGF-β and IL-4 and the suppression of Ag specific proliferation with little suppression of INF-γ. More severe EAE was found in IL-10 −/− mice than in wild type controls, however, feeding resulted in amelioration of disease severity in both groups. Orally tolerized IL-10 −/− mice had greater disease severity compared to orally tolerized wild type mice. IL-4 was present in the GALT of IL-10 −/− mice and up-regulation of TGF-β was detected in the lamina propria of fed mice. These results demonstrate that IL-10 is not required for the induction of low dose oral tolerance but is required for the regulation of INF-γ which affects severity of disease in tolerized mice.