Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: γ Activating and inhibitory Fcγ receptors in rheumatoid arthritis: from treatment to targeted therapies. | Available online http content 9 4 106 Editorial Activating and inhibitory Fey receptors in rheumatoid arthritis from treatment to targeted therapies Joel AG van Roon Rheumatology Clinical Immunology University Medical Center Utrecht Heidelberglaan 3584 CX Utrecht The Netherlands Corresponding author Joel AG van Roon Published 20 August 2007 This article is online at http content 9 4 106 2007 BioMed Central Ltd Arthritis Research Therapy 2007 9 106 doi ar2224 See related research article by Magnusson et al. http content 9 3 R51 Abstract Fcy receptors FcyRs bind the constant Fc region of IgG molecules. IgG antigen-containing immune complexes elicit a variety of effector functions in cells that express activating FcyRs. Because activating FcyRs are present on cells from the innate immune system such as dendritic cells monocytes macrophages and granulocytes these IgG receptors form a crucial link between the innate and the acquired immune systems. Recently the ability to detect the inhibitory FcyRIIb on cells has indicated an imbalance between activating and inhibitory FcyRs in rheumatoid arthritis. This progress offers an opportunity to study modulation of FcyR balance and could stimulate development of FcyR-directed immunotherapy. Activating Fcy receptors FcyRs FcyRI FcyRIIa FcyRIIIa and FcyRIIIb carry activation signalling motifs intracellularly which upon binding of IgG antigen-containing immune complexes can induce phagocytosis antigen presentation antibody-dependent cell mediated cytotoxicity and complement-mediated lysis and cytokine secretion. Expression of FcyRIIb which carries an inhibitory signalling motif downregulates effector functions upon binding of IgG-containing immune complexes thereby preventing proinflammatory responses mediated by activating FcyRs. Studies of surface expression of the inhibitory FcyRIIb in humans have for some time been hampered by
