By their interaction with IgG immune complexes, FcgR and complement link innate and adaptive immunity, showing functional redundancy. In complement-deficient mice, IgG downstream effector functions are often impaired, as well as adaptive immunity. Based on a variety of model systems using FcgR-knockout mice, it has been concluded that FcgRs are also key regulators of innate and adaptive immunity; however, several of the model systems underpinning these conclusions suffer from flawed experimental design. To address this issue, we generated a novel mouse model deficient for all FcgRs (FcgRI/II/III/IV 2 / 2 mice). These mice displayed normal development and lymphoid and myeloid ontogeny. Although IgG effector pathways were impaired, adaptive immune responses to a variety of challenges, including bacterial infection and IgG immune complexes, were not. Like FcgRIIb-deficient mice, FcgRI/II/III/IV 2 / 2 mice developed higher Ab titers but no autoantibodies. These observations indicate a redundant role for activating FcgRs in the modulation of the adaptive immune response in vivo. We conclude that FcgRs are downstream IgG effector molecules with a restricted role in the ontogeny and maintenance of the immune system, as well as the regulation of adaptive immunity.