FcγRI-Deficient Mice Show Multiple Alterations to Inflammatory and Immune Responses

AbstractThe inactivation of the mouse high-affinity IgG Fc receptor FcγRI resulted in a wide range of defects in antibody Fc-dependent functions. These studies showed the primary importance of FcγRI in endocytosis of monomeric IgG, kinetics, and extent of phagocytosis of immune complexes, in macrophage-based ADCC, and in immune complex-dependent antigen presentation to primed T cells. In the absence of FcγRI, antibody responses were elevated, implying the removal of a control point by the deletion of FcγRI. In addition, FcR-γ chain-deficient mice were found to express partially functional FcγRI. Thus, FcγRI is an early participant in Fc-dependent cell activation and in the development of immune responses