ArticleCirculation. Cardiovascular genetics2012
Role of activating FcγR gene polymorphisms in Kawasaki disease susceptibility and intravenous immunoglobulin response.
Article in Circulation. Cardiovascular genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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53 citing papers in PubMed, 81 citations in OpenAlex.
- Trial
- The Autophagy-Inflammasome Axis as a Molecular Switch: From Persistent Inflammation to Vascular Remodeling in IVIG-Resistant Kawasaki Disease.International journal of molecular sciences · 2026Review
- Single Nucleotide Polymorphisms and Their Association with Coronary Artery Aneurysms and IVIG Resistance in Kawasaki Disease in Ireland.Pediatric cardiology · 2026Article
- Etiology Model of Kawasaki Disease and Multisystem Inflammatory Syndromes: Mast Cell Activation.Current issues in molecular biology · 2026Article
- Identification of programmed cell death and mitochondria correlated biomarkers for Kawasaki disease by integrated bioinformatics and machine-learning algorithms with RT-qPCR verification.Frontiers in genetics · 2026Article
- Endothelial Dysfunction: Molecular Mechanisms and Therapeutic Strategies in Kawasaki Disease.International journal of molecular sciences · 2024Review
- Neutrophil diversity and function in health and disease.Signal transduction and targeted therapy · 2024Review
- Pharmacogenomics of coronary artery response to intravenous gamma globulin in kawasaki disease.NPJ genomic medicine · 2024Article
- Article
- Intravenous Immunoglobulin in Kawasaki Disease-Evolution and Pathogenic Mechanisms.Diagnostics (Basel, Switzerland) · 2023Review
- Pharmacogenomics of intravenous immunoglobulin response in Kawasaki disease.Frontiers in immunology · 2023Article
- Seasonality and geographical distribution of Kawasaki disease among Black children in the Southeast United States.Frontiers in pediatrics · 2023Article
- The Associated of the Risk of IVIG Resistance in Kawasaki Disease withJournal of inflammation research · 2022Article
- Predictive model based on gene and laboratory data for intravenous immunoglobulin resistance in Kawasaki disease in a Chinese population.Pediatric rheumatology online journal · 2021Article
- Kawasaki Disease and Clinical Outcome Disparities Among Black Children.The Journal of pediatrics · 2021Article
- Identification of increased expression of activating Fc receptors and novel findings regarding distinct IgE and IgM receptors in Kawasaki disease.Pediatric research · 2021Article
- Anti-inflammatory Treatment of Kawasaki Disease: Comparison of Current Guidelines and Perspectives.Frontiers in medicine · 2021Review
- Epigenetics in Kawasaki Disease.Frontiers in pediatrics · 2021Review
- Homozygous ofFrontiers in genetics · 2021Article
- Convalescent plasma in Covid-19: Possible mechanisms of action.Autoimmunity reviews · 2020Review
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10 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundA functional polymorphism in the inhibitory IgG-Fc receptor gene FcγRIIB influences intravenous immunoglobulin (IVIG) response in Kawasaki disease (KD), a vasculitis preferentially affecting the coronary arteries in children. We tested the hypothesis that the polymorphisms in the activating receptors (FcγRIIA, FcγRIIIA, and FcγRIIIB) also influence susceptibility, IVIG treatment response, and coronary artery disease in patients with KD. METHODS AND
resultsWe genotyped polymorphisms in the activating FcγRIIA, FcγRIIIA, and FcγRIIIB using pyrosequencing in 443 patients with KD, including 266 trios and 150 single parent-child pairs, in northwest United States and genetically determined race with 155 ancestry informative markers. We used family-based association to test for transmission disequilibrium and further generated pseudosibling controls for comparisons with the cases. The FcγRIIA-131H variant showed an association with KD (P=0.001) with an additive odds ratio (OR) of 1.51 (95% CI, 1.16-1.96; P=0.002) for the primary combined population, which persisted in both white (P=0.04) and Asian (P=0.01) subgroups and is consistent with the recent genome-wide association study. We also identified overtransmission of the FcγRIIIB neutrophil antigen 1 (NA1) variant among IVIG nonresponders (P=0.0002) and specifically to white IVIG nonresponders (P=0.007). ORs for overall and white nonresponders were 3.67 (95% CI, 1.75-7.66; P=0.0006) and 3.60 (95% CI, 1.34-9.70; P=0.01), respectively. Excess NA1 transmission also occurred in patients with KD with coronary artery disease (OR(additive), 2.13; 95% CI, 1.11-4.0; P=0.02).
conclusionsA common variation in FcγRIIA is associated with increased KD susceptibility. The FcγRIIIB-NA1 variant, which confers higher affinity for IgG than the NA2 variant, is a determining factor for treatment response. These activating FcγRs play an important role in KD pathogenesis and the IVIG antiinflammatory mechanism.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.