B cells are important as antigen presenting cells for induction of MHC-restricted arthritis in transgenic mice

Veena Taneja, Christopher J. Krco, Marshall D. Behrens, Harvinder S. Luthra, Marie M. Griffiths, Chella S. David

Research output: Contribution to journalArticle

22 Scopus citations

Abstract

Rheumatoid arthritis and its animal model, collagen-induced arthritis, are known as a T and B cell dependent disease. To analyze the role of B cells in arthritis, we generated B cell deficient (μMT) mice carrying HLA-DQ8 as transgene, Aβo.DQ8.μmt mice. HLA-DQ8 transgenic mice (Aβo.DQ8) are susceptible to collagen induced arthritis, an animal model for inflammatory arthritis. Deletion of IgM gene led to the absence of B cells while T cells were comparable to Aβo.DQ8 mice. Arthritis and autoantibodies was completely abrogated in B cell deficient DQ8 mice. T cell response and proinflammatory cytokine production in response to type II collagen and its derived peptides in vitro was significantly decreased despite an increased number of Mac-1 positive cells in DQ8.μmt mice compared to DQ8 mice suggesting B cells could be important for antigen presentation as well. In vitro substitution of B cells from wild type mice restored the response in DQ8.μmt mice. B cells could also present CII-derived peptides to antigen-specific DQ8-restricted hybridomas reinforcing the role of B cells in presentation of antigens to T cells. The data suggest that B cells can be involved in pathogenesis of arthritis by producing autoantibodies and antigen presentation.

Original languageEnglish (US)
Pages (from-to)2988-2996
Number of pages9
JournalMolecular Immunology
Volume44
Issue number11
DOIs
StatePublished - Apr 1 2007

Keywords

  • Antigen presentation
  • Autoantibodies
  • B cells
  • Rheumatoid arthritis
  • Transgenic/knockout mice

ASJC Scopus subject areas

  • Immunology
  • Molecular Biology

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