ArticleInflammatory bowel diseases2018
Enhanced Contribution of HLA in Pediatric Onset Ulcerative Colitis.
Article in Inflammatory bowel diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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
24 citing papers in PubMed, 49 citations in OpenAlex.
- Clinical and biological predictors of response to standardised paediatric colitis therapy (PROTECT): a multicentre inception cohort study.Lancet (London, England) · 2019Trial
- Shared CD4+ T cell receptor specificity groups in Crohn's disease and ulcerative colitis.JCI insight · 2026Article
- Potential Risk Factors and Therapeutic Targets for Dilated Cardiomyopathy Identified Through Mendelian Randomization Analysis.Journal of the American Heart Association · 2026Article
- Immune-microbe interactions in pediatric ulcerative colitis: clinical features, pathogenesis, and novel targeted therapeutic strategies.Frontiers in immunology · 2026Review
- Review
- Exploring the omnigenic architecture of selected complex traits.American journal of human genetics · 2025Article
- Genetic evidence for causal links between type 1 diabetes and autoimmune liver diseases.Diabetology & metabolic syndrome · 2025Article
- Article
- Molecular Insight into the Role of HLA Genotypes in Immunogenicity and Secondary Refractoriness to Anti-TNF Therapy in IBD Patients.International journal of molecular sciences · 2025Review
- Clinical and Genetic Characteristics of Pediatric Patients with Inflammatory Bowel Disease Transitioning to Adult Medicine: A Single-Center Ten-Year Experience.Journal of clinical medicine · 2025Article
- Post-genome-wide association study dissects genetic vulnerability and risk gene expression of Sjögren's disease for cardiovascular disease.Journal of translational medicine · 2025Article
- Mendelian Randomization Assessment of the Genetic Effects of Lipid-Lowering Drugs on Digestive System Cancers.Food science & nutrition · 2025Article
- Association between human blood metabolome and risk of myocarditis: a mendelian randomization study.Scientific reports · 2024Article
- Non-targeted metabolomics revealed novel links between serum metabolites and primary ovarian insufficiency: a Mendelian randomization study.Frontiers in endocrinology · 2024Article
- Precision medicine in inflammatory bowel disease.Precision clinical medicine · 2023Review
- Longitudinal DNA methylation profiling of the rectal mucosa identifies cell-specific signatures of disease status, severity and clinical outcomes in ulcerative colitis cell-specific DNA methylation signatures of UC.Clinical epigenetics · 2023Article
- An Extremes of Phenotype Approach Confirms Significant Genetic Heterogeneity in Patients with Ulcerative Colitis.Journal of Crohn's & colitis · 2023Article
- GPR35 acts a dual role and therapeutic target in inflammation.Frontiers in immunology · 2023Review
- Clinical and Host Biological Factors Predict Colectomy Risk in Children Newly Diagnosed With Ulcerative Colitis.Inflammatory bowel diseases · 2022Article
- GPR35 in Intestinal Diseases: From Risk Gene to Function.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
30 authors at 20 institutions in 2 countries.
Funding
Abstract
Background: The genetic contributions to pediatric onset ulcerative colitis (UC), characterized by severe disease and extensive colonic involvement, are largely unknown. In adult onset UC, Genome Wide Association Study (GWAS) has identified numerous loci, most of which have a modest susceptibility risk (OR 0.84-1.14), with the exception of the human leukocyte antigen (HLA) region on Chromosome 6 (OR 3.59). Method: To study the genetic contribution to exclusive pediatric onset UC, a GWAS was performed on 466 cases with 2099 healthy controls using UK Biobank array. SNP2HLA was used to impute classical HLA alleles and their corresponding amino acids, and the results are compared with adult onset UC. Results: HLA explained the almost entire association signal, dominated with 191 single nucleotide polymorphisms (SNPs) (p = 5 x 10-8 to 5 x 10-10). Although very small effects, established SNPs in adult onset UC loci had similar direction and magnitude in pediatric onset UC. SNP2HLA imputation identified HLA-DRB1*0103 (odds ratio [OR] = 6.941, p = 1.92*10-13) as the most significant association for pediatric UC compared with adult onset UC (OR = 3.59). Further conditioning showed independent effects for HLA-DRB1*1301 (OR = 2.25, p = 7.92*10-9) and another SNP rs17188113 (OR = 0.48, p = 7.56*10-9). Two HLA-DRB1 causal alleles are shared with adult onset UC, while at least 2 signals are unique to pediatric UC. Subsequent stratified analyses indicated that HLA-DRB1*0103 has stronger association for extensive disease (E4: OR = 8.28, p = 4.66x10-10) and female gender (OR = 8.85, p = 4.82x10-13). Conclusion: In pediatric onset UC, the HLA explains almost the entire genetic associations. In addition, the HLA association is approximately twice as strong in pediatric UC compared with adults, due to a combination of novel and shared effects. We speculate the paramount importance of antigenic stimulation either by infectious or noninfectious stimuli as a causal event in pediatric UC onset.
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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.