ArticleEuropean journal of human genetics : EJHG2010
Evidence for both copy number and allelic (NA1/NA2) risk at the FCGR3B locus in systemic lupus erythematosus.
Article in European journal of human genetics : EJHG, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 60 citations in OpenAlex.
- Comprehensive Assessment of the Association between FCGRs polymorphisms and the risk of systemic lupus erythematosus: Evidence from a Meta-Analysis.Scientific reports · 2016Pooled it
- Association between FCGR3B copy number variations and susceptibility to autoimmune diseases: a meta-analysis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2015Pooled it
- Bronchial epithelial transcriptomics and experimental validation reveal asthma severity-related neutrophilc signatures and potential treatments.Communications biology · 2024Article
- Immunogenetics of Lupus Erythematosus.Advances in experimental medicine and biology · 2022Article
- Article
- Aberrant Non-Coding RNA Expression in Patients with Systemic Lupus Erythematosus: Consequences for Immune Dysfunctions and Tissue Damage.Biomolecules · 2020Review
- Article
- Multiple Variables at the Leukocyte Cell Surface Impact Fc γ Receptor-Dependent Mechanisms.Frontiers in immunology · 2019Review
- Low copy number of FCGR3B is associated with lupus nephritis in a Chinese population.Experimental and therapeutic medicine · 2017Article
- Understanding the Genomic Structure of Copy-Number Variation of the Low-Affinity Fcγ Receptor Region Allows Confirmation of the Association of FCGR3B Deletion with Rheumatoid Arthritis.Human mutation · 2017Article
- Association analysis of copy numbers of FC-gamma receptor genes for rheumatoid arthritis and other immune-mediated phenotypes.European journal of human genetics : EJHG · 2016Article
- The role of Fc receptors in HIV prevention and therapy.Immunological reviews · 2015Review
- Complex and multi-allelic copy number variation in human disease.Briefings in functional genomics · 2015Review
- Genetics and pathogenesis of systemic lupus erythematosus and lupus nephritis.Nature reviews. Nephrology · 2015Review
- Clinical implications of copy number variations in autoimmune disorders.The Korean journal of internal medicine · 2015Review
- Hardy-Weinberg equilibrium revisited for inferences on genotypes featuring allele and copy-number variations.Scientific reports · 2015Article
- Association of FCGR3A and FCGR3B copy number variations with systemic lupus erythematosus and rheumatoid arthritis in Taiwanese patients.Arthritis & rheumatology (Hoboken, N.J.) · 2014Article
- Fcγ receptor IIIa single-nucleotide polymorphisms and haplotypes affect human IgG binding and are associated with lupus nephritis in African Americans.Arthritis & rheumatology (Hoboken, N.J.) · 2014Article
- Immunomodulation by IVIg and the Role of Fc-Gamma Receptors: Classic Mechanisms of Action after all?Frontiers in immunology · 2014Review
- Targeting the endothelial progenitor cell surface proteome to identify novel mechanisms that mediate angiogenic efficacy in a rodent model of vascular disease.Physiological genomics · 2013Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The Fcgamma-receptor locus on chromosome 1q23 shows copy-number variation (CNV), and it has previously been shown that individuals with reduced numbers of copies of the Fcgamma-receptor-IIIB gene (FCGR3B) have an increased risk of developing systemic lupus erythematosus (SLE). It is not understood whether the association arises from FCGR3B (CD16b) itself, is observed because of linkage disequilibrium with actual causal alleles and/or is an effect of CNV on flanking FCGR genes. Thus, we extended this previous work by genotyping the FCGR3B alleles NA1/NA2 and re-assaying CNV using a paralogue ratio test assay in a family study (365 families). We have developed a novel case/pseudo-control approach to analyse family data, as the phase of copy number (CN) is not known in parents and cannot always be inferred in offspring. The results, obtained by fitting logistic regression models, confirm the association of low CN of FCGR3B with SLE (P=0.04). The risk conferred by low copies (<2) was contingent on FCGR3B allotype, being greater for deletion of NA1 than the for lower-affinity NA2. The simpler model with just CN was rejected in favour of the biallelic-CN model (P=0.03). We observed a correlation (R(2)=0.75, P<0.0001) between FCGR3B CNV and neutrophil expression in both healthy controls and patients with SLE. Our results suggest that one mechanism by which CNV at this locus confers disease risk is directly as a result of reduced FcgammaRIIIb function, either because of reduced expression (related to CNV) or because of reduced affinity for its ligand (NA1/NA2 allotype).
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Registered trials
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.