Circulating immune complexes are implicated in the pathogenesis of rheumatic immune disorders and the interaction of these immune complexes with IgG Fc receptors (FcγR) seems to be a determining step in the initiation of the inflammatory process. Mice deficient in the FcRγ‐chain, and thus lacking multiple FcR, have previously been shown to be protected from collagen‐induced arthritis (CIA). However, the relative contribution of the different FcγR has not been identified. In this study, we investigated the expression and contribution of FcγRIII, the activating low‐affinity FcγR in the development of CIA. Wild‐type and FcγRIII‐deficient DBA/1 (FcγRIII^–/–) mice were immunized with bovine collagen type II (BCII) in Freund's complete adjuvant and arthritis development was evaluated by clinical and histological examinations. We found that FcγRIII^–/– mice developed virtually no arthritis in contrast to wild‐type mice, the majority of which developed severe CIA. Although resistant to CIA, the humoral and cellular responses to BCII in FcγRIII^–/– mice were similar to that seen in wild‐type controls. FcγRIII expression was studied on sections from normal joints of FcγRII‐deficient DBA/1 mice stained with the mAb 2.4G2, specific for FcγRII and FcγRIII. FcγRIII was demonstrated in cells of thelining and sublining layer of the synovial membrane. We conclude that development of CIA requires FcγRIII and that expression of FcγRIII on synovial cells may contribute to the antibody‐triggered inflammation in joints.