Low-affinity Fcgamma receptors, autoimmunity and infection
- PMID: 19674504
- DOI: 10.1017/S1462399409001161
Low-affinity Fcgamma receptors, autoimmunity and infection
Abstract
Low-affinity Fcgamma receptors (FcgammaRs) 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 FcgammaRs are activatory, there is also an inhibitory FcgammaR that, when bound to IgG immune complexes, is able to downregulate the effects of both the activatory FcgammaRs and the B cell receptor. This review discusses the role of the low-affinity FcgammaRs in a balanced immune response and how perturbations in FcgammaR function result in susceptibility to infection or autoimmunity.
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