Abstract
We have shown previously that intranasal administration of encephalitogenic peptides in soluble form to H-2u and H-2s mice affords protection from experimental autoimmune encephalomyelitis (EAE). Here we demonstrate that this method of disease protection can be induced in C57BL/6 mice by administration of the soluble peptide 35-55 from myelin oligodendrocyte glycoprotein. This protective effect was demonstrated by the evaluation of both clinical EAE scores and central nervous system histopathology; the latter showing minimal inflammatory infiltrates in treated mice. The employment of an IL-10-/- congenic strain allowed an appraisal of the involvement of IL-10 in this process. The lack of disease protection in these mice clearly demonstrates the non-redundant role of IL-10 in this process.