Murine low‐affinity receptors for IgG, FcγRII and FcγRIII, differ by their distinct capacities in mediating down‐regulation or activation of cellular effector functions, respectively. In this study, antibodies detecting the mouse Ly‐17.1 / 2 alloantigen system are demonstrated to be specific for FcγRII with no cross‐reactivities to other FcγR, including FcγRIII. Using these FcγRII‐specific monoclonal antibodies (mAb), the significance of FcγRII inhibition of FcγRIII was examined in two models of autoantibody [autoimmune hemolytic anemia (AIHA)]‐ and IgG immune complex‐induced (Arthus reaction) inflammation in C57BL / 6 mice in comparison with FcγRII^{– / –} and FcγRIII^{– / –} mice. Our results demonstrate that both FcγRIII and FcγRII contributed to the binding of erythrocytes opsonized with the pathogenic IgG1 autoreactive anti‐murine red blood cell antibody 105‐2H. However, the functional blocking with anti‐FcγRII mAb in C57BL / 6 mice and the lack of FcγRII expression in FcγRII^{– / –} mice, which both lowered the threshold level of FcγRIII‐triggered phagocytosis in vitro, did not results in enhanced disease development of 105‐2H mAb‐induced AIHA in vivo. This was in sharp contrast to cutaneous Arthus reaction, where FcγRIII‐mediated activation was inhibited by FcγRII. Together these results show that murine AIHA is markedly different from other FcγR‐dependent inflammatory diseases where FcγRIII is normally counterregulated by FcγRII.