Similar to previous studies of lupus-prone mice performed in our laboratory (31), we found that B cell deficiency of FcγRIIB led to an increase in PCs, without an increase in the fraction of ANA+ IgG PCs, suggestive of increased B cell activation and PC differentiation rather than an antigen-specific tolerance defect. This evidence concerns the gene FCGR2B and systemic lupus erythematosus.