Evidence map›Paper›PMID 18559452›Full record

ArticleThe Journal of experimental medicine2008

Copy number of FCGR3B, which is associated with systemic lupus erythematosus, correlates with protein expression and immune complex uptake.

Lisa C Willcocks, Paul A Lyons, Menna R Clatworthy, James I Robinson, Wanling Yang, Stephen A Newland, Vincent Plagnol, Naomi N McGovern, Alison M Condliffe, Edwin R Chilvers and 7 more

Open access · bronzeAbstract readMulticenter Study
In one paragraph

Article in The Journal of experimental medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed, 4 pooled it
9.0field-weighted citation impact, top 2% 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

120 citing papers in PubMed, 4 syntheses or guidelines pooled it, 228 citations in OpenAlex.

  1. Pooled it
  2. 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
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  7. Article
  8. Experimental and therapeutic medicine · 2026
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  9. Review
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  14. Pitfalls When Determining HNA-1 Genotypes and Finding Novel Alleles.International journal of molecular sciences · 2024
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60 more citing papers are in PubMed but not listed here.

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

17 authors at 6 institutions in 4 countries.

Lisa C WillcocksDepartment of Medical Genetics, Cambridge Institute for Medical Research, University of Cambridge, CB2 0XY, England, UK.
Paul A Lyons
Menna R Clatworthy
James I Robinson
Wanling Yang
Stephen A Newland
Vincent Plagnol
Naomi N McGovern
Alison M Condliffe
Edwin R Chilvers
Dwomoa Adu
Elaine C Jolly
Richard Watts
Yu Lung Lau
Ann W Morgan
Gerard Nash
Kenneth G C Smith
Institute for Medical Research · MYQueen Mary Hospital · CNSt James's University Hospital · GBUniversity of Birmingham · GBUniversity of Cambridge · GBUniversity of East Anglia · GB

Funding

Medical Research Council G0500450Wellcome Trust 081020
6 · The paper itself

Abstract

Copy number (CN) variation (CNV) has been shown to be common in regions of the genome coding for immune-related genes, and thus impacts upon polygenic autoimmunity. Low CN of FCGR3B has recently been associated with systemic lupus erythematosus (SLE). FcgammaRIIIb is a glycosylphosphatidylinositol-linked, low affinity receptor for IgG found predominantly on human neutrophils. We present novel data demonstrating that both in a family with FcgammaRIIIb-deficiency and in the normal population, FCGR3B CNV correlates with protein expression, with neutrophil uptake of and adherence to immune complexes, and with soluble serum FcgammaRIIIb. Reduced FcgammaRIIIb expression is thus likely to contribute to the impaired clearance of immune complexes, which is a feature of SLE, explaining the association between low FCGR3B CNV and SLE that we have confirmed in a Caucasian population. In contrast, antineutrophil cytoplasmic antibody-associated systemic vasculitis (AASV), a disease not associated with immune complex deposition, is associated with high FCGR3B CN. Thus, we define a role for FCGR3B CNV in immune complex clearance, a function that may explain why low FCGR3B CNV is associated with SLE, but not AASV. This is the first report of an association between disease-related gene CNV and variation in protein expression and function that may contribute to autoimmune disease susceptibility.

Indexed as

Genetic Predisposition to DiseaseGenetic VariationAntibodies, Antineutrophil CytoplasmicAntigen-Antibody ComplexAutoimmunityFemaleGene DosageGene Expression RegulationGPI-Linked ProteinsHumansLupus Erythematosus, SystemicMaleNeutrophilsReceptors, IgGVasculitisWhite PeopleAntibodies, Antineutrophil CytoplasmicAntigen-Antibody ComplexFCGR3B protein, humanGPI-Linked ProteinsReceptors, IgG

Identifiers

PMID18559452
PMCPMC2442635
OpenAlexW2145047609

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.