ArticlePloS one2013
A refined study of FCRL genes from a genome-wide association study for Graves' disease.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Trial
- Immune Cell-specific Genetic Regulation in Graves' Disease: An Integrative Mendelian Randomization Study.Endocrine, metabolic & immune disorders drug targets · 2026Article
- FcRL1, a New B-Cell-Activating Co-Receptor.International journal of molecular sciences · 2025Review
- Graves disease: latest understanding of pathogenesis and treatment options.Nature reviews. Endocrinology · 2024Review
- The Increased FCRL mRNA Expression in Patients with Graves' Disease Is Associated with Hyperthyroidism (But Not with Positive Thyroid Antibodies).Journal of clinical medicine · 2024Article
- Motif-Raptor: a cell type-specific and transcription factor centric approach for post-GWAS prioritization of causal regulators.Bioinformatics (Oxford, England) · 2021Article
- Variants of Novel Immunomodulatory Fc Receptor Like 5 Gene Are Associated With Multiple Sclerosis Susceptibility in the Polish Population.Frontiers in neurology · 2021Article
- The rs6427384 and rs6692977 Single Nucleotide Polymorphisms of the Fc Receptor-Like 5 (FCRL5) Gene and the Risk of Ankylosing Spondylitis: A Case Control Study in a Single Center in China.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Candidate gene associations reveal sex-specific Graves' disease risk alleles among Chinese Han populations.Molecular genetics & genomic medicine · 2020Article
- Pooled genome wide association detects association upstream of FCRL3 with Graves' disease.BMC genomics · 2016Article
- Fc Receptor-Like Proteins in Pathophysiology of B-cell Disorder.Journal of clinical & cellular immunology · 2016Article
- Four FCRL3 Gene Polymorphisms (FCRL3_3, _5, _6, _8) Confer Susceptibility to Multiple Sclerosis: Results from a Case-Control Study.Molecular neurobiology · 2016Article
- Significant Association Between Fc Receptor-Like 3 Polymorphisms (-1901A>G and -658C>T) and Neuromyelitis Optica (NMO) Susceptibility in the Chinese Population.Molecular neurobiology · 2016Article
- Article
- Genetic associations of FCRL3 polymorphisms with the susceptibility of Graves ophthalmopathy in a Chinese population.International journal of clinical and experimental medicine · 2015Article
- Correlation between single nucleotide polymorphism of FCRL-3 gene and Graves' disease in Han population of northern Anhui province, China.International journal of clinical and experimental medicine · 2015Article
- FCRL3 gene polymorphisms confer autoimmunity risk for allergic rhinitis in a Chinese Han population.PloS one · 2015Article
- Emerging roles for the FCRL family members in lymphocyte biology and disease.Current topics in microbiology and immunology · 2014Review
Corrections and comments
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Authors and funding
20 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To pinpoint the exact location of the etiological variant/s present at 1q21.1 harboring FCRL1-5 and CD5L genes, we carried out a refined association study in the entire FCRL region in 1,536 patients with Graves' disease (GD) and 1,516 sex-matched controls by imputation analysis, logistic regression, and cis-eQTL analysis. Among 516 SNPs with P<0.05 in the initial GWAS scan, the strongest signals associated with GD and correlated to FCRL3 expression were located at a cluster of SNPs including rs7528684 and rs3761959. And the allele-specific effects for rs3761959 and rs7528684 on FCRL3 expression level revealed that the risk alleles A of rs3761959 and C of rs7528684 were correlated with the elevated expression level of FCRL3 whether in PBMCs or its subsets, especially in CD19(+) B cells and CD8(+) T subsets. Next, the combined analysis with 5,300 GD cases and 4,916 control individuals confirmed FCRL3 was a susceptibility gene of GD in Chinese Han populations, and rs3761959 and rs7528684 met the genome-wide association significance level (P(combined) = 2.27×10(-12) and 7.11×10(-13), respectively). Moreover, the haplotypes with the risk allele A of rs3761959 and risk allele C of rs7528684 were associated with GD risk. Finally, our epigenetic analysis suggested the disease-associated C allele of rs7528684 increased affinity for NF-KB transcription factor. Above data indicated that FCRL3 gene and its proxy SNP rs7528684 may be involved in the pathogenesis of GD by excessive inhibiting B cell receptor signaling and the impairment of suppressing function of Tregs.
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