SynthesisPLoS genetics2011
A meta-analysis of genome-wide association scans identifies IL18RAP, PTPN2, TAGAP, and PUS10 as shared risk loci for Crohn's disease and celiac disease.
Synthesis in PLoS genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 9 of them syntheses that pooled it.
What it found
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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.
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Who cites it
112 citing papers in PubMed, 9 syntheses or guidelines pooled it, 225 citations in OpenAlex.
- Pooled it
- A cross-disease meta-GWAS identifies four new susceptibility loci shared between systemic sclerosis and Crohn's disease.Scientific reports · 2020Pooled it
- Association of LPP and TAGAP Polymorphisms with Celiac Disease Risk: A Meta-Analysis.International journal of environmental research and public health · 2017Pooled it
- Interleukin and interleukin receptor gene polymorphisms in inflammatory bowel diseases susceptibility.World journal of gastroenterology · 2014Pooled it
- Genetic comorbidities in Parkinson's disease.Human molecular genetics · 2014Pooled it
- A systemic sclerosis and systemic lupus erythematosus pan-meta-GWAS reveals new shared susceptibility loci.Human molecular genetics · 2013Pooled it
- Association of celiac disease genes with inflammatory bowel disease in Finnish and Swedish patients.Genes and immunity · 2012Pooled it
- Combined analysis of genome-wide association studies for Crohn disease and psoriasis identifies seven shared susceptibility loci.American journal of human genetics · 2012Pooled it
- A comprehensive analysis of shared loci between systemic lupus erythematosus (SLE) and sixteen autoimmune diseases reveals limited genetic overlap.PLoS genetics · 2011Pooled it
- Polygenic Risk Scores Show Distinct Genetic Architectures of IBD-Associated Comorbidities.Digestive diseases and sciences · 2026Article
- Integrated DNA methylome and transcriptome signatures of lung CD4ERJ open research · 2026Article
- Multi-omics analysis identifies PUS7 as an immune modulator driving NETs-mediated macrophage polarization in pancreatic cancer.Clinical and translational medicine · 2026Article
- Deletion of Ptpn2 in B cells promotes autoimmunity via TLR and JAK/STAT signaling.JCI insight · 2025Article
- The IL-18 receptor is expressed on murine small-intestinal enterochromaffin cells and executes a recovery program upon injury.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- Shared Genetics in Celiac Disease and Inflammatory Bowel Disease Specify a Greater Role for Intestinal Epithelial Cells.International journal of molecular sciences · 2025Review
- TAGAP restrains myeloid and T cell activation in inflammatory bowel disease.Frontiers in immunology · 2025Article
- Enhancing the apo protein tyrosine phosphatase non-receptor type 2 crystal soaking strategy through inhibitor-accessible binding sites.Acta crystallographica. Section F, Structural biology communications · 2024Article
- Enhanced Risk of Gastroesophageal Reflux Disease and Esophageal Complications in the Ulcerative Colitis Population.Journal of clinical medicine · 2024Article
- The molecular basis of tRNA selectivity by human pseudouridine synthase 3.Molecular cell · 2024Article
52 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 11 institutions in 5 countries.
Funding
Abstract
Crohn's disease (CD) and celiac disease (CelD) are chronic intestinal inflammatory diseases, involving genetic and environmental factors in their pathogenesis. The two diseases can co-occur within families, and studies suggest that CelD patients have a higher risk to develop CD than the general population. These observations suggest that CD and CelD may share common genetic risk loci. Two such shared loci, IL18RAP and PTPN2, have already been identified independently in these two diseases. The aim of our study was to explicitly identify shared risk loci for these diseases by combining results from genome-wide association study (GWAS) datasets of CD and CelD. Specifically, GWAS results from CelD (768 cases, 1,422 controls) and CD (3,230 cases, 4,829 controls) were combined in a meta-analysis. Nine independent regions had nominal association p-value <1.0 x 10⁻⁵ in this meta-analysis and showed evidence of association to the individual diseases in the original scans (p-value < 1 x 10⁻² in CelD and < 1 x 10⁻³ in CD). These include the two previously reported shared loci, IL18RAP and PTPN2, with p-values of 3.37 x 10⁻⁸ and 6.39 x 10⁻⁹, respectively, in the meta-analysis. The other seven had not been reported as shared loci and thus were tested in additional CelD (3,149 cases and 4,714 controls) and CD (1,835 cases and 1,669 controls) cohorts. Two of these loci, TAGAP and PUS10, showed significant evidence of replication (Bonferroni corrected p-values <0.0071) in the combined CelD and CD replication cohorts and were firmly established as shared risk loci of genome-wide significance, with overall combined p-values of 1.55 x 10⁻¹⁰ and 1.38 x 10⁻¹¹ respectively. Through a meta-analysis of GWAS data from CD and CelD, we have identified four shared risk loci: PTPN2, IL18RAP, TAGAP, and PUS10. The combined analysis of the two datasets provided the power, lacking in the individual GWAS for single diseases, to detect shared loci with a relatively small effect.
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Registered trials
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.