B cells limit epitope spreading and reduce severity of EAE induced with PLP peptide in BALB/c mice

Jeri Anne Lyons, Michael J. Ramsbottom, Robert J. Mikesell, Anne H. Cross

Research output: Contribution to journalArticle

19 Scopus citations

Abstract

The role of B cells and antibody in experimental autoimmune encephalomyelitis (EAE) appears to differ based on the identity and state (protein vs. encephalitogenic peptide) of the inducing antigen and the strain of mouse utilized. The involvement of B cells in the induction of EAE by peptides of proteolipid protein (PLP) in BALB/c mice was investigated. Wild-type and B cell-deficient (B cell-/-) mice on the BALB/c background were immunized with overlapping PLP peptides, and the disease course was followed. Although incidence and onset of PLP180-199-induced EAE was similar in WT and B cell-/- mice, the clinical course was more severe in B cell-/- mice. During acute disease, proliferation and interferon-γ production by lymphoid cells from both strains were similar and were elicited predominantly in response to the immunizing antigen. However, during chronic disease lymphoid cells isolated from B cell-/- mice proliferated to a greater extent and produced more interferon-γ in response to the overlapping peptide PLP185-206 and to the smaller internal peptide PLP185-199 than did WT mice. These data suggest that B cells regulate PLP-induced EAE in BALB/c mice through control of epitope spreading.

Original languageEnglish
Pages (from-to)149-155
Number of pages7
JournalJournal of Autoimmunity
Volume31
Issue number2
DOIs
StatePublished - Sep 1 2008

Keywords

  • Antibody
  • B cells
  • Epitope spreading
  • Experimental autoimmune encephalomyelitis
  • Proteolipid protein

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