Low-affinity Fcγ receptors, autoimmunity and infection

Abstract

Low-affinity Fcγ receptors (FcγRs) mediate the effects of immunoglobulin G (IgG) antibodies on leukocytes, including recruitment to inflammatory lesions, phagocytosis, antibody-dependent cellular cytotoxicity, release of inflammatory mediators and regulation of B cell activation. These functions are an important part of the mammalian response to infection, but if deployed inappropriately can cause autoimmune disease. Although most FcγRs are activatory, there is also an inhibitory FcγR that, when bound to IgG immune complexes, is able to downregulate the effects of both the activatory FcγRs and the B cell receptor. This review discusses the role of the low-affinity FcγRs in a balanced immune response and how perturbations in FcγR function result in susceptibility to infection or autoimmunity.