The key roles of the complement cascade and cellular Fcγ receptors in the innate and adaptive immune system are well documented. Recognition of soluble or cell-bound IgG-containing immune complexes by either of these two respective effector systems leads to a complex series of separate and non-overlapping inflammatory reactions and cytotoxic processes, each of which serves to remove or destroy opsonized microorganisms or targeted tumor cells. Alternatively, in autoimmune diseases these reactions mediate severe pathologies which are manifested in local or systemic inflammation as well as in tissue injury. For some time, it appeared that these two effector systems functioned independently and did not communicate; however, increasing evidence reveals synergy and feedback control between these two systems. Indeed, danger signals can alert one system leading to cross-communication and cooperation with the other to efficiently eliminate the threat. On the other hand, undesired and deleterious inflammation can be controlled by FcγR-mediated suppression of complement.