Resistance to development of collagen-induced arthritis in C57BL/6 mice is due to a defect in secondary, but not in primary, immune response

J Clin Immunol. 2004 Sep;24(5):481-91. doi: 10.1023/B:JOCI.0000040919.16739.44.

Abstract

Collagen-induced arthritis (CIA) is a rodent model of human rheumatoid arthritis. Mice of the H-2(q) (DBA/1J) background are highly susceptible to disease whereas mice of the H-2(b) (C57BL/6, B6) background are resistant. To determine why B6 mice are resistant to disease induction, we systematically analyzed T and B cell immune responses in B6 mice, compared to DBA/1J mice, following immunization with bovine type II collagen (CII). We found that both strains showed similar T cell proliferation and cytokine responses and similar levels of anti-CII antibodies (Abs) at day 12 or day 14 of initial immunization (primary immune response), however, those B6 mice that did not develop arthritis showed a significant defect in T cell responses and significantly lower levels of anti-CII Abs following secondary boosting immunization (day 35 of initial immunization, secondary immune response) compared to DBA/1J mice. Our results define for the first time that a defective secondary immune responses in B6 mice leads to the resistance of CIA.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antibodies / immunology
  • Arthritis, Experimental / immunology*
  • Cell Division / immunology
  • Collagen / immunology*
  • Cytokines / metabolism
  • Immunity, Active / immunology
  • Immunity, Innate / immunology*
  • Joints / immunology
  • Joints / pathology
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred DBA
  • T-Lymphocyte Subsets / metabolism
  • T-Lymphocytes / immunology
  • Th1 Cells / metabolism

Substances

  • Antibodies
  • Cytokines
  • Collagen