Evidence map›Paper›PMID 20854658›Full record

ArticleArthritis research & therapy2010

Overlapping genetic susceptibility variants between three autoimmune disorders: rheumatoid arthritis, type 1 diabetes and coeliac disease.

Stephen Eyre, Anne Hinks, John Bowes, Edward Flynn, Paul Martin, Anthony G Wilson, Ann W Morgan, Paul Emery, Sophia Steer, Lynne J Hocking and 8 more

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 6 pooled it
7.0field-weighted citation impact, top 3% 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

53 citing papers in PubMed, 6 syntheses or guidelines pooled it, 116 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Association of LPP and TAGAP Polymorphisms with Celiac Disease Risk: A Meta-Analysis.International journal of environmental research and public health · 2017
    Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Behçet-like Syndromes: A Comprehensive Review.Dermatopathology (Basel, Switzerland) · 2026
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 7 institutions in 1 country.

Stephen EyreArthritis Research UK, Epidemiology Unit, Stopford Building, Oxford Road, The University of Manchester, Manchester M13 9PT, UK. steve.eyre@manchester.ac.uk
Anne Hinks
John Bowes
Edward Flynn
Paul Martin
Anthony G Wilson
Ann W Morgan
Paul Emery
Sophia Steer
Lynne J Hocking
David M Reid
Pille Harrison
Paul Wordsworth
Yorkshire Early Arthritis Consortium
Biologics in RA Control Consortium
Wendy Thomson
Jane Worthington
Anne Barton
University of Manchester · GBUniversity of Aberdeen · GBUniversity of Leeds · GBKing's College Hospital NHS Foundation Trust · GBNIHR Oxford Musculoskeletal Biomedical Research Centre · GBUniversity of Oxford · GBUniversity of Sheffield · GB

Funding

Arthritis Research UK 17552Versus Arthritis 18475
6 · The paper itself

Abstract

introductionGenome wide association studies, replicated by numerous well powered validation studies, have revealed a large number of loci likely to play a role in susceptibility to many multifactorial diseases. It is now well established that some of these loci are shared between diseases with similar aetiology. For example, a number of autoimmune diseases have been associated with variants in the PTPN22, TNFAIP3 and CTLA4 genes. Here we have attempted to define overlapping genetic variants between rheumatoid arthritis (RA), type 1 diabetes (T1D) and coeliac disease (CeD).

methodsWe selected eight SNPs previously identified as being associated with CeD and six T1D-associated SNPs for validation in a sample of 3,962 RA patients and 3,531 controls. Genotyping was performed using the Sequenom MassArray platform and comparison of genotype and allele frequencies between cases and controls was undertaken. A trend test P-value < 0.004 was regarded as significant.

resultsWe found statistically significant evidence for association of the TAGAP locus with RA (P = 5.0 × 10-4). A marker at one other locus, C1QTNF6, previously associated with T1D, showed nominal association with RA in the current study but did not remain statistically significant at the corrected threshold.

conclusionsIn exploring the overlap between T1D, CeD and RA, there is strong evidence that variation within the TAGAP gene is associated with all three autoimmune diseases. Interestingly a number of loci appear to be specific to one of the three diseases currently studied suggesting that they may play a role in determining the particular autoimmune phenotype at presentation.

Indexed as

Polymorphism, Single NucleotideAdultArthritis, RheumatoidCeliac DiseaseDiabetes Mellitus, Type 1FemaleGenetic Predisposition to DiseaseGenotypeGTPase-Activating ProteinsHumansMaleMiddle AgedOligonucleotide Array Sequence AnalysisGTPase-Activating ProteinsTAGAP protein, human

Identifiers

PMID20854658
PMCPMC2991006
OpenAlexW2163584865

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.