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• W2013310648 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." @default.
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• W2013310648 date "1999-11-01" @default.
• W2013310648 modified "2023-10-05" @default.
• W2013310648 title "B cells are critical to induction of experimental allergic encephalomyelitis by protein but not by a short encephalitogenic peptide" @default.
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• W2013310648 doi "https://doi.org/10.1002/(sici)1521-4141(199911)29:11<3432::aid-immu3432>3.0.co;2-2" @default.
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