Evidence map›Paper›PMID 16356189›Full record

ArticleArthritis research & therapy2006

Analysis of Fcgamma receptor haplotypes in rheumatoid arthritis: FCGR3A remains a major susceptibility gene at this locus, with an additional contribution from FCGR3B.

Ann W Morgan, Jennifer H Barrett, Bridget Griffiths, Deepak Subramanian, Jim I Robinson, Viki H Keyte, Manir Ali, Elizabeth A Jones, Robert W Old, Frederique Ponchel and 5 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Arthritis research & therapy, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 2 pooled it
2.0field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 46 citations in OpenAlex.

  1. Association ofFrontiers in immunology · 2025
    Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Targeting the Fc receptor in autoimmune disease.Expert opinion on therapeutic targets · 2014
    Review
  12. Human FcR polymorphism and disease.Current topics in microbiology and immunology · 2014
    Review
  13. Article
  14. Review
  15. Article
  16. Macrophages in synovial inflammation.Frontiers in immunology · 2011
    Article
  17. Article
  18. Review
  19. Review
  20. Article
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

15 authors at 6 institutions in 1 country.

Ann W MorganInstitute of Molecular Medicine, Epidemiology and Cancer Research, University of Leeds, St James's University Hospital, Beckett Street, Leeds, LS9 7TF, UK. a.w.morgan@leeds.ac.uk
Jennifer H Barrett
Bridget Griffiths
Deepak Subramanian
Jim I Robinson
Viki H Keyte
Manir Ali
Elizabeth A Jones
Robert W Old
Frederique Ponchel
Arthur W Boylston
R Deva Situnayake
Alexander F Markham
Paul Emery
John D Isaacs
St James's University Hospital · GBUniversity of Leeds · GBChapel Allerton Hospital · GBUniversity of Warwick · GBNewcastle University · GBSandwell & West Birmingham Hospitals NHS Trust · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Fcgamma receptors play important roles in the initiation and regulation of many immunological and inflammatory processes, and genetic variants (FCGR) have been associated with numerous autoimmune and infectious diseases. The data in rheumatoid arthritis (RA) are conflicting and we previously demonstrated an association between FCGR3A and RA. In view of the close molecular proximity with FCGR2A, FCGR2B and FCGR3B, additional polymorphisms within these genes and FCGR haplotypes were examined to refine the extent of association with RA. Biallelic polymorphisms in FCGR2A, FCGR2B and FCGR3B were examined for association with RA in two well characterized UK Caucasian and North Indian/Pakistani cohorts, in which FCGR3A genotyping had previously been undertaken. Haplotype frequencies and linkage disequilibrium were estimated across the FCGR locus and a model-free analysis was performed to determine association with RA. This was followed by regression analysis, allowing for phase uncertainty, to identify the particular haplotype(s) that influences disease risk. Our results reveal that FCGR2A, FCGR2B and FCGR3B were not associated with RA. The haplotype with the strongest association with RA susceptibility was the FCGR3A-FCGR3B 158V-NA2 haplotype (odds ratio 3.18, 95% confidence interval 1.13-8.92 [P = 0.03] for homozygotes compared with all genotypes). The association was stronger in the presence of nodules (odds ratio 5.03, 95% confidence interval 1.44-17.56; P = 0.01). This haplotype was also more common in North Indian/Pakistani RA patients than in control individuals, but not significantly so. Logistic regression analyses suggested that FCGR3A remained the most significant gene at this locus. The increased association with an FCGR3A-FCGR3B haplotype suggests that other polymorphic variants within FCGR3A or FCGR3B, or in linkage disequilibrium with this haplotype, may additionally contribute to disease pathogenesis.

Indexed as

Chromosomes, Human, Pair 1Antigens, CDArthritis, RheumatoidBase SequenceChromosome MappingCohort StudiesGenetic Predisposition to DiseaseGenetic VariationGenotypeGPI-Linked ProteinsHumansLinkage DisequilibriumPolymerase Chain ReactionPolymorphism, Single NucleotideReceptors, IgGReference ValuesAntigens, CDFCGR3B protein, humanGPI-Linked ProteinsReceptors, IgG

Identifiers

PMID16356189
PMCPMC1526569
OpenAlexW1768700520

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.