SynthesisCanadian journal of gastroenterology = Journal canadien de gastroenterologie2010
Replication and meta-analysis of 13,000 cases defines the risk for interleukin-23 receptor and autophagy-related 16-like 1 variants in Crohn's disease.
Synthesis in Canadian journal of gastroenterology = Journal canadien de gastroenterologie, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 5 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.
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.
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Who cites it
17 citing papers in PubMed, 5 syntheses or guidelines pooled it, 29 citations in OpenAlex.
- ATG16L1 rs2241880/T300A increases susceptibility to perianal Crohn's disease: An updated meta-analysis on inflammatory bowel disease risk and clinical outcomes.United European gastroenterology journal · 2024Pooled it
- Genetic association between IL23R rs11209026 and rs10889677 polymorphisms and risk of Crohn's disease and ulcerative colitis: evidence from 41 studies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Pooled it
- Association between ATG16L1 gene polymorphism and the risk of Crohn's disease.The Journal of international medical research · 2017Pooled it
- IL-23R mutation is associated with ulcerative colitis: A systemic review and meta-analysis.Oncotarget · 2017Pooled it
- Association of Interleukin-23 receptor gene polymorphisms with susceptibility to Crohn's disease: A meta-analysis.Scientific reports · 2015Pooled it
- Multi-omics in Crohn's disease: New insights from inside.Computational and structural biotechnology journal · 2023Review
- Bacterial Translocation as Inflammatory Driver in Crohn's Disease.Frontiers in cell and developmental biology · 2021Review
- Effector T Helper Cell Subsets in Inflammatory Bowel Diseases.Frontiers in immunology · 2018Review
- Disease Phenotype, Activity and Clinical Course Prediction Based on C-Reactive Protein Levels at Diagnosis in Patients with Crohn's Disease: Results from the CONNECT Study.Gut and liver · 2016Article
- The IL-23-IL-17 immune axis: from mechanisms to therapeutic testing.Nature reviews. Immunology · 2014Review
- Detection of Mycobacterium avium subspecies paratuberculosis in patients with Crohn's disease is unrelated to the presence of single nucleotide polymorphisms rs2241880 (ATG16L1) and rs10045431 (IL12B).Medical microbiology and immunology · 2014Article
- Endoplasmic reticulum aminopeptidase 1 and interleukin-23 receptor in ankylosing spondylitis.Current rheumatology reports · 2012Review
- Autophagy in immunity: implications in etiology of autoimmune/autoinflammatory diseases.Autophagy · 2012Review
- The role of autophagy in Crohn's disease.Cells · 2012Article
- Sex differences in disease risk from reported genome-wide association study findings.Human genetics · 2012Article
- A "crossomics" study analysing variability of different components in peripheral blood of healthy caucasoid individuals.PloS one · 2012Article
- Pulmonary-intestinal cross-talk in mucosal inflammatory disease.Mucosal immunology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
objectiveVariants in the interleukin-23 receptor (IL23R) and the autophagy-related 16-like 1 (ATG16L1) genes have been associated with an increased risk of Crohn's disease (CD). Both genes were identified through genome-wide association scans and subsequent studies have validated these associations. To assess the effect size of these variants, an independent case-control association study and meta-analysis were performed.
methodsBritish Caucasian subjects with inflammatory bowel disease (n=500) and 877 ethnically matched controls were genotyped for the disease-associated variants in IL23R and ATG16L1. In addition, meta-analyses of 12,991 patients and 14,598 controls, and 11,909 patients and 15,798 controls, were conducted on independently published data for the associations between IL23R and ATG16L1 variants and CD, respectively.
resultsIn the present cohort, both susceptibility variants showed highly significant associations, including IL23R (rs11209026, P=0.0006; OR 0.37; 95% CI 0.21 to 0.67) and ATG16L1 (rs2241880, P=0.0017; OR 1.36; 95% CI 1.12 to 1.66). The meta-analysis based on the random effects model showed similar combined effects for rs11209026 (n=26, OR 0.41; 95% CI 0.37 to 0.46) and rs2241880 (n=25, OR 1.33; 95% CI 1.28 to 1.39). There was no statistically significant gene-gene interaction between caspase recruitment domain (CARD15) variants and the IL23R or ATG16L1 polymorphisms (P=0.44 and P=0.24, respectively).
conclusionThe present cohort and meta-analysis provides strong evidence that, in addition to CARD15, polymorphisms in both IL23R and ATG16L1 alter susceptibility to CD and that these effects are consistent across all populations of European ancestry; however, only ATG16L1 is relevant to inflammatory bowel disease in the Asian population.
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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.