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

Jeri Anne Lyons, Manuel San, Mary Pat Happ, Anne H. Cross

Research output: Contribution to journalArticlepeer-review

224 Scopus citations

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.

Original languageEnglish
Pages (from-to)3432-3439
Number of pages8
JournalEuropean Journal of Immunology
Volume29
Issue number11
DOIs
StatePublished - 1999

Keywords

  • Antigen
  • Antigen processing
  • Autoimmunity
  • Multiple sclerosis
  • Myelin oligodendrocyte glycoprotein

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