Amelioration of EAE by a cryptic epitope of myelin oligodendrocyte glycoprotein

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.

Antigen recognition in autoimmune diabetes: a novel pathway underlying disease initiation

“…42 The importance of T cells with a “type-B” feature has been highlighted in other autoimmune diseases in mice and humans. 43–48 A notable example is a recent study that characterized hypocretin-specific CD4 T cells in patients with narcolepsy; most of these T cells recognized only the exogenous peptides not those post protein-processing. 49…”