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Updated: Jun 21, 2026

Interrogating Individual Autoreactive Germinal Centers by Photoactivation in a Mixed Chimeric Model of Autoimmunity
Published on: April 11, 2019
Low-affinity Fcgamma receptors, autoimmunity and infection
Lisa C Willcocks1, Kenneth G C Smith, Menna R Clatworthy
1Cambridge Institute for Medical Research and Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge, CB2 0XY, UK.
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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