The Journal of Experimental Medicine
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Published online 1 May 2000.
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© The Rockefeller University Press, 0022-1007/2000/5/1611/ $5.00
The Journal of Experimental Medicine, Volume 191, Number 9, May 1, 2000 1611-1616

Brief Definitive Report

Induction and Suppression of Collagen-Induced Arthritis Is Dependent on Distinct Fc{gamma} Receptors

Sandra Kleinaua, Pernilla Martinssona, and Birgitta Heymana

a Department of Genetics and Pathology, Uppsala University, S-75185 Uppsala, Sweden
Department of Genetics and Pathology, Uppsala University, S-75185 Uppsala, Sweden.46-18-55893146-18-663836

sandra.kleinau{at}genpat.uu.se

Receptors for immunoglobulin (Ig)G (Fc{gamma}Rs) are important for the antibody-mediated effector functions of the immune system. Fc{gamma}RI and Fc{gamma}RIII trigger cell activation through a common {gamma} chain, whereas Fc{gamma}RII acts as a negative regulator of antibody production and immune complex–triggered activation. Here we describe the in vivo consequences of Fc{gamma}R deficiency in a mouse model of human rheumatoid arthritis. FcR{gamma} chain–deficient mice on arthritis-susceptible DBA/1 background were immunized with collagen for induction of collagen-induced arthritis. The DBA/1 mice lacking FcR{gamma} chain were protected from collagen-induced arthritis in contrast to wild-type mice, although both groups produced similar levels of IgG anticollagen antibodies. In comparison, DBA/1 mice lacking Fc{gamma}RII developed an augmented IgG anticollagen response and arthritis. These observations suggest a crucial role of Fc{gamma}RI and Fc{gamma}RIII in triggering autoimmune arthritis.

Key Words: autoimmunity • mice • knock-outs • immunoglobulin receptor • antibodies

© 2000 The Rockefeller University Press


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