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      Human Low-Affinity IgG Receptor FcγRIIA Polymorphism H131R Associates with Subclinical Atherosclerosis and Increased Platelet Activity in Systemic Lupus Erythematosus

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          Abstract

          Background:

          Systemic lupus erythematosus (SLE) is a complex autoimmune disease associated with an elevated risk for premature cardiovascular disease. Platelets express receptors contributing to inflammation and immunity including FcγRIIA, the low affinity receptor of the Fc portion of IgG antibodies. The variation at a single amino acid substitution, H131R, in the extracellular binding domain alters the affinity for IgG, which may account for individual variation in platelet activity and platelet mediated disease.

          Objectives:

          This study was performed to investigate the association between FcγRIIA genotype, preclinical atherosclerosis, platelet reactivity, and vascular health.

          Methods:

          FcγRIIA was genotyped in 80 SLE patients and 30 healthy controls. Carotid ultrasound plaque, soluble E-selectin, and platelet aggregability were evaluated in SLE and matched controls.

          Results:

          Carotid plaque was significantly more prevalent in SLE patients carrying a variant allele compared to those who were homozygous ancestral (58% vs. 25%, P=0.04). In contrast, prevalent carotid plaque was not associated with genotype in controls. Consistently, SLE variant FcγRIIA carriers vs. ancestral had a significant increase in the levels of soluble E-selectin, which was not observed in controls. Monocyte and leukocyte-platelet aggregation and platelet aggregation in response to submaximal agonist stimulation were significantly elevated in SLE patients with the variant vs. ancestral genotype.

          Conclusions:

          Carotid ultrasound plaque, soluble E-selectin levels and platelet activity were more frequently prevalent in SLE patients carrying variant FcγRIIA. The interplay between FcγRIIA-mediated platelet activation and endothelial cells might represent a mechanism underlying the pathogenesis of cardiovascular disease in SLE patients.

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          Author and article information

          Journal
          101170508
          30450
          J Thromb Haemost
          J. Thromb. Haemost.
          Journal of thrombosis and haemostasis : JTH
          1538-7933
          1538-7836
          14 January 2019
          13 February 2019
          March 2019
          01 March 2020
          : 17
          : 3
          : 532-537
          Affiliations
          [* ]Department of Medicine, Division of Rheumatology, NYU Langone Medical Center, NY, NY
          []Department of Medicine, Division of Cardiology, NYU Langone Medical Center, NY, NY
          Author notes

          Addendum

          R. Clancy, J. P. Buyon, and J. S. Berger had the concept

          R. Clancy, S. E. Rasmussen, N. Bornkamp, N. Allen, R. Dann, H. Reynolds carried out the experiments.

          H. El Bannoudi, H. Reynolds, R. Clancy, J. P. Buyon, and J.S. Berger drafted and edited the manuscript.

          Address for Correspondence: Jeffrey S. Berger M.D., Associate Professor of Medicine and Surgery, New York University School of Medicine, Tel: 212-263-4004, jeffrey.berger@ 123456nyumc.org
          Article
          PMC6440197 PMC6440197 6440197 nihpa1006531
          10.1111/jth.14385
          6440197
          30638300
          368057c3-bf1a-4dae-a1b6-ba1cadeeaed3
          History
          Categories
          Article

          systemic Lupus Erythematosus (SLE),platelets,FcγRIIA,cardiovascular disease,Atherosclerosis

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