Neutrophil accumulation is a hallmark of immune complex-mediated inflammatory disorders. Current models of neutrophil recruitment envision the capture of circulating neutrophils by activated endothelial cells. We now demonstrate that immobilized immune complexes alone support the rapid attachment of neutrophils, under physiologic flow conditions. Initial cell tethering requires the low-affinity Fcγ receptor IIIB (FcγRIIIB), and the β₂ integrins are additionally required for the subsequent shear-resistant adhesion. The attachment function of FcγRIIIB may be facilitated by its observed presentation on neutrophil microvilli. In vivo, in a model of acute antiglomerular basement membrane nephritis in which immune complexes are accessible to circulating neutrophils, FcγRIII-deficient mice had a significant reduction in neutrophil recruitment. Thus, the interaction of immune complexes with FcγRIII may mediate early neutrophil recruitment in immune complex-mediated inflammation.