Crosslinking of Fc γ receptor II B (FcγRIIB) and the BCR by immune complexes (IC) can downregulate antigen‐specific B‐cell responses. Accordingly, FcγRIIB deficiencies have been associated with B‐cell hyperactivity in patients with systemic lupus erythematosus and mouse models of lupus. However, we have previously shown that murine IgG2a‐autoreactive AM14 B cells respond robustly to chromatin‐associated IC through a mechanism dependent on both the BCR and the endosomal TLR9, despite FcγRIIB coexpression. To further evaluate the potential contribution of FcγRIIB to the regulation of autoreactive B cells, we have now compared the IC‐triggered responses of FcγRIIB‐deficient and FcγRIIB‐sufficient AM14 B cells. We find that FcγRIIB‐deficient cells respond significantly better than FcγRIIB‐sufficient cells when stimulated with DNA IC that incorporate low‐affinity TLR9 ligand (CG‐poor dsDNA fragments). AM14 B cells also respond to RNA‐associated IC through BCR/TLR7 coengagement, but such BCR/TLR7‐dependent responses are normally highly dependent on IFN‐α costimulation. However, we now show that AM14 FcγRIIB^−/− B cells are very effectively activated by RNA IC without supplemental IFN‐α priming. These results demonstrate that FcγRIIB can effectively modulate both BCR/TLR9 and BCR/TLR7 endosomal‐dependent activation of autoreactive B cells.