Amelioration of EAE by a cryptic epitope of myelin oligodendrocyte glycoprotein
Jeri A Lyons1, Melissa M Riter2, Alaa M Almatrook2
1Department of Biomedical Sciences, University of Wisconsin - Milwaukee, Milwaukee, WI 53211, USA; Department of Neurology and Neurosurgery, Washington University School of Medicine, Saint Louis, MO, USA 63110.
Abstract:
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.
