Low-affinity Fcγ receptors, autoimmunity and infection

Lisa C. Willcocks; Kenneth G.C. Smith; Menna R. Clatworthy

doi:10.1017/S1462399409001161

Low-affinity Fcγ receptors, autoimmunity and infection

Published online by Cambridge University Press: 13 August 2009

Lisa C. Willcocks ,

Kenneth G.C. Smith and

Menna R. Clatworthy

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Lisa C. Willcocks: Affiliation:
Cambridge Institute for Medical Research and Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge, CB2 0XY, UK.
Kenneth G.C. Smith: Affiliation:
Cambridge Institute for Medical Research and Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge, CB2 0XY, UK.
Menna R. Clatworthy*: Affiliation:
Cambridge Institute for Medical Research and Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge, CB2 0XY, UK.
*: *Corresponding author: Menna R. Clatworthy, Cambridge Institute for Medical Research and Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Hills Road, Cambridge, CB2 0XY, UK. Tel: +44 1223 762639; Fax: +44 1223 762645; E-mail: mrc38@cam.ac.uk

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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.

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Type: Review Article
Information: Expert Reviews in Molecular Medicine , Volume 11 , July 2009 , e24

DOI: https://doi.org/10.1017/S1462399409001161 [Opens in a new window]
Copyright: Copyright © Cambridge University Press 2009

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