Evidence map›Paper›PMID 20454450›Full record

ArticlePloS one2010

Evidence for STAT4 as a common autoimmune gene: rs7574865 is associated with colonic Crohn's disease and early disease onset.

Jürgen Glas, Julia Seiderer, Melinda Nagy, Christoph Fries, Florian Beigel, Maria Weidinger, Simone Pfennig, Wolfram Klein, Jörg T Epplen, Peter Lohse and 7 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Genetic association betweenFrontiers in genetics · 2025
    Article
  3. STAT4 gene polymorphisms in human diseases.Frontiers in immunology · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Protein kinase 2 (CK2) controls CD4Mucosal immunology · 2020
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Host-microbiome interaction in Crohn's disease: A familiar or familial issue?World journal of gastrointestinal pathophysiology · 2015
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Polymorphisms ofBiomedical reports · 2013
    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

17 authors at 6 institutions in 1 country.

Jürgen GlasDepartment of Medicine II-Grosshadern, University of Munich, Munich, Germany.
Julia Seiderer
Melinda Nagy
Christoph Fries
Florian Beigel
Maria Weidinger
Simone Pfennig
Wolfram Klein
Jörg T Epplen
Peter Lohse
Matthias Folwaczny
Burkhard Göke
Thomas Ochsenkühn
Julia Diegelmann
Bertram Müller-Myhsok
Darina Roeske
Stephan Brand
Ludwig-Maximilians-Universität München · DELMU Klinikum · DEMax Planck Institute of Psychiatry · DERuhr University Bochum · DETechnical University of Munich · DERWTH Aachen University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecent studies demonstrated an association of STAT4 variants with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), indicating that multiple autoimmune diseases share common susceptibility genes. We therefore investigated the influence of STAT4 variants on the susceptibility and phenotype of inflammatory bowel diseases (IBD) in a large patient and control cohort. METHODOLOGY/PRINCIPAL

findingsGenomic DNA from 2704 individuals of Caucasian origin including 857 patients with Crohn's disease (CD), 464 patients with ulcerative colitis (UC), and 1383 healthy, unrelated controls was analyzed for seven SNPs in the STAT4 gene (rs11889341, rs7574865, rs7568275, rs8179673, rs10181656, rs7582694, rs10174238). In addition, a detailed genotype-phenotype analysis was performed. Our analysis revealed an association of the STAT4 SNP rs7574865 with overall decreased susceptibility to CD (p = 0.047, OR 0.86 [95% CI 0.74-0.99]). However, compared to CD patients carrying the wild type genotype, the STAT4 SNP rs7574865 was significantly associated with early CD onset (p = 0.021) and colonic CD (p = 0.008; OR = 4.60, 95% CI 1.63-12.96). For two other STAT4 variants, there was a trend towards protection against CD susceptibility (rs7568275, p = 0.058, OR 0.86 [95% CI 0.74-1.00]; rs10174238, p = 0.057, OR 0.86 [95% CI 0.75-1.00]). In contrast, we did not observe any association with UC susceptibility. Evidence for weak gene-gene interaction of STAT4 with the IL23R SNP rs11209026 was lost after Bonferroni correction. CONCLUSIONS/SIGNIFICANCE: Our results identified the STAT4 SNP rs7574865 as a disease-modifying gene variant in colonic CD. However, in contrast to SLE and RA, the effect of rs7574865 on CD susceptibility is only weak.

Indexed as

Age of OnsetAutoimmune DiseasesCase-Control StudiesCrohn DiseaseGenetic Predisposition to DiseaseHumansInflammatory Bowel DiseasesPolymorphism, Single NucleotideReceptors, InterleukinSTAT4 Transcription FactorIL23R protein, humanReceptors, InterleukinSTAT4 Transcription Factor

Identifiers

PMID20454450
PMCPMC2861592
OpenAlexW1973994873

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.