Amelioration of EAE by a cryptic epitope of myelin oligodendrocyte glycoprotein

Previous work demonstrated that EAE induced by recombinant human MOG was B cell-dependent. Data presented here reveal a T cell response to MOG61–85 in human rMOG-immunized B cell−/− mice not observed in WT mice. Further study revealed this peptide to be a cryptic epitope in WT mice. Co-immunization of B cell−/− mice with MOG35–55 and MOG61–85 peptides led to less severe disease compared to mice immunized with MOG35–55 alone. Disease amelioration was associated with decreased production of Interferon-γ by lymph node cells. Thus, MOG61–85 represents a protective epitope to human rMOG induced EAE in B cell−/− mice. [Display omitted] •MOG61–85 represents a cryptic epitope of rMOG in wild-type C57BL/6 mice.•MOG61–85 is naturally processed in B cell-deficient C57BL/6 mice.•Immunization with MOG35–55+MOG61–85 ameliorates clinical EAE in B cell−/−mice•Processing of MOG61–85 is regulated by an antibody-dependent mechanism