Evidence map›Paper›PMID 25521225›Full record

SynthesisGenes and immunity2015

Meta-analysis of the TNFAIP3 region in psoriasis reveals a risk haplotype that is distinct from other autoimmune diseases.

J Nititham, K E Taylor, R Gupta, H Chen, R Ahn, J Liu, M Seielstad, A Ma, A M Bowcock, L A Criswell and 2 more

Open access · bronzeAbstract readMeta-Analysis
In one paragraph

Synthesis in Genes and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-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

22 citing papers in PubMed, 35 citations in OpenAlex.

  1. Co-Occurrence ofInternational journal of molecular sciences · 2025
    Article
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  4. Sequential immunotherapy: towards cures for autoimmunity.Nature reviews. Drug discovery · 2024
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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

12 authors at 5 institutions in 5 countries.

J Nititham1] Department of Dermatology, University of California San Francisco, San Francisco, CA, USA [2] Department of Medicine, Rosalind Russell Medical Research Center for Arthritis, University of California San Francisco, San Francisco, CA, USA.
K E TaylorDepartment of Medicine, Rosalind Russell Medical Research Center for Arthritis, University of California San Francisco, San Francisco, CA, USA.
R GuptaDepartment of Dermatology, University of California San Francisco, San Francisco, CA, USA.
H ChenDepartment of Gastroenterology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Institute of Digestive Diseases, Shanghai, China.
R AhnDepartment of Dermatology, University of California San Francisco, San Francisco, CA, USA.
J Liu1] Department of Human Genetics, Genome Institute of Singapore, A*STAR, Singapore, Singapore [2] Saw Swee Hock School of Public Health, National University of Singapore, Singapore, Singapore [3] School of Life Sciences, Anhui Medical University, Hefei, China.
M Seielstad1] Department of Dermatology, University of California San Francisco, San Francisco, CA, USA [2] Blood Systems Research Institute, San Francisco, CA, USA.
A MaDivision of Gastroenterology, University of California San Francisco, San Francisco, CA, USA.
A M BowcockDepartment of Cancer Genomics, Imperial College of London, London, UK.
L A CriswellDepartment of Medicine, Rosalind Russell Medical Research Center for Arthritis, University of California San Francisco, San Francisco, CA, USA.
M StahleUnit of Dermatology and Venereology, Department of Medicine, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.
W LiaoDepartment of Dermatology, University of California San Francisco, San Francisco, CA, USA.ORCID 0000000178836439
University of California, San Francisco · USAgency for Science, Technology and Research · SGGenomics (United Kingdom) · GBKarolinska University Hospital · SEShanghai Jiao Tong University · CN

Funding

Genome-Wide SNP Association in PsoriasisR01AR050266 · NIAMS · WASHINGTON UNIVERSITY · PI BOWCOCK, ANNE MARY · 2007 to 2016
$5.7M
Identification of Causal Variants in PsoriasisR01AR065174 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LIAO, WILSON · 2013 to 2016
$1.8M
Genetic Analysis of the TNF Pathway in PsoriasisK08AR057763 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LIAO, WILSON · 2010 to 2014
$599k
NIAMS NIH HHS 2R01 AR050266NIAMS NIH HHS K08 AR057763NIAMS NIH HHS K08AR057763NIAMS NIH HHS R01 AR050266NIAMS NIH HHS R01 AR065174NIAMS NIH HHS R01AR065174Wellcome TrustWellcome Trust 076113Wellcome Trust 085475
6 · The paper itself

Abstract

Tumor necrosis factor alpha-inducible protein 3 (TNFAIP3) encodes a ubiquitin-modifying protein, A20, that is a critical regulator of inflammatory responses. TNFAIP3 polymorphisms are associated with the susceptibility to multiple autoimmune diseases (AIDs) including psoriasis, systemic lupus erythematosus, rheumatoid arthritis, systemic sclerosis and celiac disease. In order to refine the TNFAIP3 association signal in psoriasis and identify candidate causal variants, we performed imputation and meta-analysis of the TNFAIP3 region in five European ancestry cohorts totaling 4704 psoriasis cases and 7805 controls. We identified 49 variants whose significance exceeded a corrected Bonferroni threshold, with the top variant being rs582757 (P = 6.07 × 10(-12), odds ratio (OR) = 1.23). Conditional analysis revealed a suggestive independent association at rs6918329 (P(cond) = 7.22 × 10(-5), OR = 1.15). Functional annotation of the top variants identified several with a strong evidence of regulatory potential and several within long noncoding RNAs. Analysis of TNFAIP3 haplotypes revealed that the psoriasis risk haplotype is distinct from other AIDs. Overall, our findings identify novel candidate causal variants of TNFAIP3 in psoriasis and highlight the complex genetic architecture of this locus in autoimmune susceptibility.

Indexed as

Autoimmune DiseasesCohort StudiesFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyHaplotypesHumansIntracellular Signaling Peptides and ProteinsMalePolymorphism, Single NucleotideProteinsPsoriasisIntracellular Signaling Peptides and ProteinsProteinsTNIP3 protein, human

Identifiers

PMID25521225
PMCPMC4526682
OpenAlexW2050695256

What OpenQuestion holds

Textmetadata
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Registered trials

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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.