Activation of regulatory cells suppresses experimental allergic encephalomyelitis via secretion of IL-10

Suppression of CD4(+) Th1 cell-mediated autoimmune disease via immune devia tion is an attractive potential therapeutic approach. CD4+ Th2 T cells spec ific for myelin basic protein, induced by immunization of young adult male SJL mice, suppress or modify the progression of CNS autoimmune disease, Thi s report demonstrates that activation of non-neuroantigen-specific Th2 cell s is sufficient to suppress both clinical and histological experimental all ergic encephalomyelitis (EAE). Th2 cells were obtained following immunizati on of male SJL mice with keyhole limpet hemocyanin, Transfer of these cells did not modify EAE, a model of human multiple sclerosis, in the absence of cognate Ag. Disease suppression was obtained following adoptive transfer a nd subcutaneous immunization. Suppression was not due to the deletion of my elin basic protein-specific T cells, but resulted from the presence of IL-1 0 as demonstrated by the inhibition of Th2-mediated EAE suppression via pas sive transfer with either anti-IL-10 or anti-IL-10R mAb, These data demonst rate that peripheral activation of a CD4(+) Th2 population specific for an Ag not expressed in the CNS modifies CNS autoimmune disease via LL-EO, Thes e data suggest that either peripheral activation or direct administration o f IL-XO may be of benefit in treating Th1-mediated autoimmune diseases.