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Induction and Suppression of Collagen-induced Arthritis Is Dependent on Distinct Fc Receptors

Correspondence to: Sandra Kleinau, Department of Genetics and Pathology, Uppsala University, S-75185 Uppsala, Sweden. Tel:46-18-663836 Fax:46-18-558931 E-mail:sandra.kleinau{at}genpat.uu.se.

Receptors for immunoglobulin (Ig)G (FcRs) are important for the antibody-mediated effector functions of the immune system. FcRI and FcRIII trigger cell activation through a common chain, whereas FcRII acts as a negative regulator of antibody production and immune complex–triggered activation. Here we describe the in vivo consequences of FcR deficiency in a mouse model of human rheumatoid arthritis. FcR 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 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 FcRII developed an augmented IgG anticollagen response and arthritis. These observations suggest a crucial role of FcRI and FcRIII in triggering autoimmune arthritis.

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

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