Evidence map›Paper›PMID 22551723›Full record

ArticleGenes and immunity2012

Evidence that deletion at FCGR3B is a risk factor for systemic sclerosis.

C McKinney, J C A Broen, M C Vonk, L Beretta, R Hesselstrand, N Hunzelmann, G Riemekasten, R Scorza, C P Simeon, V Fonollosa and 8 more

Abstract read
PubMed Publisher
In one paragraph

Article in Genes and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 17% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. 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.] · 2015
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. The Immunogenetics of Systemic Sclerosis.Advances in experimental medicine and biology · 2022
    Article
  7. Potential Target Genes in the Development of Atrial Fibrillation: A Comprehensive Bioinformatics Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2021
    Article
  8. Review
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  10. Article
  11. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors at 12 institutions in 6 countries.

C McKinneyDepartment of Biochemistry, University of Otago, Dunedin, New Zealand.
J C A Broen
M C Vonk
L Beretta
R Hesselstrand
N Hunzelmann
G Riemekasten
R Scorza
C P Simeon
V Fonollosa
P E Carreira
N Ortego-Centeno
M A Gonzalez-Gay
P Airo
M Coenen
J Martin
T R D J Radstake
T R Merriman
Radboud University Nijmegen · NLUniversity of Milan · ITUniversity of Otago · NZVall d'Hebron Hospital Universitari · ESAzienda Socio Sanitaria Territoriale degli Spedali Civili di Brescia · ITFundación Marques de Valdecilla · ESGerman Rheumatism Research Centre · DEInstituto de Investigación Biosanitaria de Granada · ESInstituto de Parasitología y Biomedicina "López - Neyra" · ESLund University · SEResearch Institute Hospital 12 de Octubre · ESUniversity of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is increasing evidence that gene copy number (CN) variation influences clinical phenotype. The low-affinity Fc receptor 3B (FCGR3B) located in the FCGR gene cluster is a CN polymorphic gene involved in the recruitment of polymorphonuclear neutrophils to sites of inflammation and their activation. Given the genetic overlap between systemic lupus erythematosus and systemic sclerosis (SSc) and the strong evidence for FCGR3B CN in the pathology of SLE, we hypothesised that FCGR3B gene dosage influences susceptibility to SSc. We obtained FCGR3B deletion status in 777 European Caucasian cases and 1000 controls. There was an inverse relationship between FCGR3B CN and disease susceptibility. CN of ≤ 1 was a significant risk factor for SSc (OR=1.55 (1.13-2.14), P=0.007) relative to CN ≥ 2. Although requiring replication, these results suggest that impaired immune complex clearance arising from FCGR3B deficiency contributes to the pathology of SSc, and FCGR3B CN variation is a common risk factor for systemic autoimmunity.

Indexed as

Gene DeletionAutoantibodiesBase SequenceCase-Control StudiesCentromereDNA Copy Number VariationsDNA ProbesDNA Topoisomerases, Type IEuropeGene DosageGenetic Association StudiesGPI-Linked ProteinsHumansReceptors, IgGRisk FactorsScleroderma, DiffuseAutoantibodiesDNA ProbesDNA Topoisomerases, Type IFCGR3B protein, humanGPI-Linked ProteinsReceptors, IgG

Identifiers

PMID22551723
OpenAlexW2140966680

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.