In subsequent studies, the protective effect of IVIg in a mouse model of IC-mediated (K/BxN) arthritis was shown to be mediated by colony stimulating factor-1 (CSF-1)-dependent macrophages that act as sensors for IVIg and are involved in the induction of inhibitory FcγRIIB expression on CSF-1-independent effector macrophages, thereby raising the threshold for activation of these cells by auto-antibody-IC (9). Here, FCGR2B is linked to arthritic joint disease.