B cell-deficient mice do not develop type II collagen-induced arthritis (CIA).
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.
Svensson
L
L
Section for Medical Inflammation Research, CMB, Lund University, Sweden.
Jirholt
J
J
Holmdahl
R
R
Jansson
L
L
D000818:Animals; D001169:Arthritis, Experimental / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology*; D002417:Cattle; D003094:Collagen; D008213:Lymphocyte Activation / Q000187:drug effects; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D051381:Rats; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology
D003094:Collagen