IgG and Fcγ Receptors in Intestinal Immunity and Inflammation

Frontiers in Immunology

Menna R. Clatworthy¹  Tomas Castro-Dopico² 

[1] Cellular Genetics, Wellcome Sanger Institute, Hinxton, United Kingdom;Molecular Immunity Unit, MRC Laboratory of Molecular Biology, Department of Medicine, University of Cambridge, Cambridge, United Kingdom;NIHR Cambridge Biomedical Research CentreCambridge, United Kingdom;

关键词: Fcγ receptor;    IgG;    inflammatory bowel disease;    intestinal immunity;    mucosal infections;    neonatal immunity;   

DOI  :  10.3389/fimmu.2019.00805

来源: DOAJ

【 摘 要 】

Fcγ receptors (FcγR) are cell surface glycoproteins that mediate cellular effector functions of immunoglobulin G (IgG) antibodies. Genetic variation in FcγR genes can influence susceptibility to a variety of antibody-mediated autoimmune and inflammatory disorders, including systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). More recently, however, genetic studies have implicated altered FcγR signaling in the pathogenesis of inflammatory bowel disease (IBD), a condition classically associated with dysregulated innate and T cell immunity. Specifically, a variant of the activating receptor, FcγRIIA, with low affinity for IgG, confers protection against the development of ulcerative colitis, a subset of IBD, leading to a re-evaluation of the role of IgG and FcγRs in gastrointestinal tract immunity, an organ system traditionally associated with IgA. In this review, we summarize our current understanding of IgG and FcγR function at this unique host-environment interface, from the pathogenesis of colitis and defense against enteropathogens, its contribution to maternal-fetal cross-talk and susceptibility to cancer. Finally, we discuss the therapeutic implications of this information, both in terms of how FcγR signaling pathways may be targeted for the treatment of IBD and how FcγR engagement may influence the efficacy of therapeutic monoclonal antibodies in IBD.

【 授权许可】

Unknown