ArticleMediators of inflammation2015
FCGR2A Promoter Methylation and Risks for Intravenous Immunoglobulin Treatment Responses in Kawasaki Disease.
Article in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Etiology Model of Kawasaki Disease and Multisystem Inflammatory Syndromes: Mast Cell Activation.Current issues in molecular biology · 2026Article
- Multiomics approaches in Kawasaki disease: insights into pathogenesis and emerging directions for diagnosis and treatment.Clinical and experimental pediatrics · 2026Article
- NLRC4 methylation and its response to intravenous immunoglobulin therapy in Kawasaki disease: a case control study.BMC pediatrics · 2024Article
- Homozygous ofFrontiers in genetics · 2021Article
- DNA methylation biomarkers of future health outcomes in children.Molecular and cellular pediatrics · 2020Review
- Identification of aberrantly methylated differentially expressed genes targeted by differentially expressed miRNA in osteosarcoma.Annals of translational medicine · 2020Article
- Interleukin-1 Beta-Mediated Sex Differences in Kawasaki Disease Vasculitis Development and Response to Treatment.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Lower CMV and EBV Exposure in Children With Kawasaki Disease Suggests an Under-Challenged Immune System.Frontiers in pediatrics · 2020Article
- The Human FcγRII (CD32) Family of Leukocyte FcR in Health and Disease.Frontiers in immunology · 2019Review
- Prediction for Intravenous Immunoglobulin Resistance by Using Weighted Genetic Risk Score Identified From Genome-Wide Association Study in Kawasaki Disease.Circulation. Cardiovascular genetics · 2017Article
- Article
- Male-specific association of the FCGR2A His167Arg polymorphism with Kawasaki disease.PloS one · 2017Article
- [Research advances in association between vitamin D and Kawasaki disease and related mechanisms of action].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2016Review
- Major methylation alterations on the CpG markers of inflammatory immune associated genes after IVIG treatment in Kawasaki disease.BMC medical genomics · 2016Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kawasaki disease (KD) is characterized by pediatric systemic vasculitis of an unknown cause. The low affinity immunoglobulin gamma Fc region receptor II-a (FCGR2A) gene was reported to be involved in the susceptibility of KD. DNA methylation is one of the epigenetic mechanisms that control gene expression; thus, we hypothesized that methylation status of CpG islands in FCGR2A promoter associates with the susceptibility and therapeutic outcomes of Kawasaki disease. In this study, 36 KD patients and 24 healthy subjects from out-patient clinic were recruited. Eleven potential methylation sites within the targeted promoter region of FCGR2A were selected for investigation. We marked the eleven methylation sites from A to K. Our results indicated that methylation at the CpG sites G, H, and J associated with the risk of KD. CpG sites B, C, E, F, H, J, and K were found to associate with the outcomes of IVIG treatment. In addition, CpG sites G, J, and K were predicted as transcription factors binding sites for NF-kB, Myc-Max, and SP2, respectively. Our study reported a significant association among the promoter methylation of FCGR2A, susceptibility of KD, and the therapeutic outcomes of IVIG treatment. The methylation levels of CpG sites of FCGR2A gene promoter should be an important marker for optimizing IVIG therapy.
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