MOG and arthritic joint disease: Indeed, a dependence on B-cell presentation for T-cell priming has been demonstrated in protein-induced models of both arthritis and EAE.34,35 Moreover, B-cell depletion leads to diametrically opposed outcomes in the two modes of immunization: exacerbating peptide-driven EAE but suppressing protein-induced disease.35 In the protein model, high titers of pathogenic MOG-specific antibody are generated and B cells are capable of efficiently priming encephalogenic Th1 and Th17 cells.