B cell-deficient mice do not develop type II collagen-induced arthritis (CIA)

Clin Exp Immunol. 1998 Mar;111(3):521-6. doi: 10.1046/j.1365-2249.1998.00529.x.


To investigate the role of B cells in the development of CIA, a model for rheumatoid arthritis, we investigated susceptibility to CIA in mice lacking B cells due to the deletion of the IgM heavy chain gene (muMT). The muMT deletion was backcrossed into two different CIA-susceptible strains, B10.Q and B10.RIII. Two different variants of the CIA model are inducible in these strains: in B10.Q with rat type II collagen (CII) and in B10.RIII with bovine CII. Homozygous deletion of the IgM gene led to the absence of B cells and dramatically reduced immunoglobulin levels compared with wild-type mice. The deletion of IgM totally abrogated development of CIA in both strains, although the anti-CII T cell response did not differ between the muMT and wild-type controls. We conclude that B cells play a crucial role in the development of CIA.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Arthritis, Experimental / immunology*
  • B-Lymphocytes / immunology*
  • Cattle
  • Collagen*
  • Lymphocyte Activation / drug effects
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Rats
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / immunology


  • Collagen