SynthesisInflammation research : official journal of the European Histamine Research Society ... [et al.]2015
Association between FCGR3B copy number variations and susceptibility to autoimmune diseases: a meta-analysis.
Synthesis in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Association of Fc Gamma Receptor 3B Gene Copy Number Variation with Rheumatoid Arthritis Susceptibility.Genes · 2022Pooled it
- Integrated bioinformatics, machine learning, and molecular docking reveal crosstalk genes and potential drugs between periodontitis and systemic lupus erythematosus.Scientific reports · 2025Article
- Potential diagnostic markers and therapeutic targets for periodontitis with comorbid infective endocarditis based on bioinformatics and experimental analyses.Frontiers in cell and developmental biology · 2025Article
- Developing models for the diagnosing of ulcerative colitis and prognosis of anti-TNF-α non-response based on neutrophil extracellular trap-associated genes.Frontiers in immunology · 2025Article
- Vitamin D in Primary Sjogren's Syndrome (pSS) and the Identification of Novel Single-Nucleotide Polymorphisms Involved in the Development of pSS-Associated Diseases.Diagnostics (Basel, Switzerland) · 2024Review
- The 330 risk loci known for systemic lupus erythematosus (SLE): a review.Frontiers in lupus · 2024Article
- The Genetic Cross-Talk between Periodontitis and Chronic Kidney Failure Revealed by Transcriptomic Analysis.Genes · 2023Article
- Proteogenomic analysis of human cerebrospinal fluid identifies neurologically relevant regulation and informs causal proteins for Alzheimer's disease.Research square · 2023Article
- Potential Target Genes in the Development of Atrial Fibrillation: A Comprehensive Bioinformatics Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- Nonendocrine mechanisms of sex bias in rheumatic diseases.Nature reviews. Rheumatology · 2019Review
- Genetic Variation in Low-To-Medium-Affinity Fcγ Receptors: Functional Consequences, Disease Associations, and Opportunities for Personalized Medicine.Frontiers in immunology · 2019Review
- Expression, Role, and Regulation of Neutrophil Fcγ Receptors.Frontiers in immunology · 2019Review
- Observational
- FcγRIIIb Restricts Antibody-Dependent Destruction of Cancer Cells by Human Neutrophils.Frontiers in immunology · 2018Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study determined whether FCGR3B copy number variations (CNVs) were associated with susceptibility to autoimmune diseases.
methodsA meta-analysis was conducted to determine the association between FCGR3B CNVs and susceptibility to autoimmune diseases by comparing low FCGR3B CN (<2 to ≥2) and high FCGR3B CN (>2 to ≤2).
resultsIn all, 28 comparative studies from 15 reports involving 12,160 patients and 11,103 controls were included in this meta-analysis. The meta-analysis showed a significant association between low FCGR3B CN and autoimmune diseases (OR=1.496, 95% CI=1.301-1.716, p=1.0×10(-9)). Subgroup analysis according to ethnicity indicated an association between low FCGR3B CN and autoimmune diseases in Caucasians (OR=1.482, 95% CI=1.219-1.801, p=7.7×10(-6)) and Asians (OR=1.498, 95% CI=1.306-1.717, p=1.0×10(-9)). Meta-analysis according to the type of autoimmune disease indicated a significant association of low FCGR3B CN with systemic lupus erythematosus (SLE; OR=1.797, 95% CI=1.562-2.068, p<1.0×10(-9)), primary Sjogren's syndrome (pSS; OR=2.263, 95% CI=1.316-3.892, p=0.003), and Wegener's granulomatosis (WG; OR=1.973, 95% CI=1.178-3.302, p=0.010), but not with rheumatoid arthritis (RA; OR=1.333, 95% CI=0.947-1.877, p=0.099). However, the meta-analysis showed no association between high FCGR3B CN and SLE, RA, pSS, and WG.
conclusionsThus, the results of this meta-analysis indicated that low FCGR3B CN increased susceptibility to autoimmune diseases, especially SLE, pSS, and WG.
Indexed as
Identifiers
What OpenQuestion holds
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.