B cells are critical to induction of experimental allergic encephalomyelitis by protein but not by a short encephalitogenic peptide

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Abstract
While the pathology of multiple sclerosis implicates a role for B cells and antibodies in the disease process, results from animal models have yielded conflicting results. To further characterize the role of B cells in experimental allergic encephalomyelitis (EAE), wild‐type and B cell‐deficient C57BL / 6 mice were immunized with either a recombinant form of myelin oligodendrocyte glycoprotein (MOG) or with the encephalitogenic MOG(35 – 55) peptide. B cell‐deficient mice did not develop EAE when immunized with MOG, although they were susceptible to MOG(35 – 55)‐induced disease. In contrast, wild‐type mice were fully susceptible to both MOG and MOG(35 – 55)‐induced EAE. B cell‐deficient mice immunized with MOG were primed to the encephalitogenic MOG(35 – 55) epitope, as their spleen cells responded with Th1 cytokine production in a fashion similar to WT cells when challenged in vitro with MOG protein or MOG(35 – 55) peptide. These results demonstrate that the form of inducing antigen (protein vs. peptide) plays a role in the pathogenesis of EAE and may be relevant when applying results from the EAE model to multiple sclerosis.