ArticleProceedings of the National Academy of Sciences of the United States of America2009
From the Cover: CD39 deletion exacerbates experimental murine colitis and human polymorphisms increase susceptibility to inflammatory bowel disease.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 187 papers.
What it found
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The trial behind it
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Who cites it
187 citing papers in PubMed, 280 citations in OpenAlex.
- Characterization of human CD39+ Th17 cells with suppressor activity and modulation in inflammatory bowel disease.PloS one · 2014Trial
- Compartment-specific PPARδ activity controls the outcome of cancer-immune cell competition and immunotherapy efficacy.Nature immunology · 2026Article
- Regulation of Tph cell differentiation via farnesoid X receptor of dendritic cells in inflammatory bowel disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Apremilast therapy increases CD39Rheumatology international · 2026Observational
- Tumor Suppressor CADM1 Protects Against Colitis in Inflammatory Bowel Disease Through Enhancing Epithelial Regeneration.International journal of molecular sciences · 2026Article
- Dysregulation of CD39/Ectonucleoside Triphosphate Diphosphohydrolase 1 Causes Urinary Bladder Dysfunction with Abnormal Smooth Muscle Contractility.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Anti-Inflammatory Effects ofFood science & nutrition · 2026Article
- UC-associated autoantibodies to αvβ6 inhibit mucosal TGFβ activation and predispose to intestinal inflammation.bioRxiv : the preprint server for biology · 2026Article
- Purinergic signaling in the gut neuro-glial-immune axis: mechanisms of homeostasis, inflammation, and gastrointestinal dysfunction.Frontiers in gastroenterology (Lausanne, Switzerland) · 2026Review
- Berberine suppresses colon inflammation via integrated modulation of host metabolism, microbial ecology, and innate immune signaling.Theranostics · 2026Article
- The P2X7 Receptor Promotes Intestinal Fibrosis by Modulating the Gut Microbiota and the Inflammasome.Cellular and molecular gastroenterology and hepatology · 2026Article
- Damage response signaling by the extracellular adenosine pathway: control of infection outcome during host aging.mSphere · 2025Review
- S1P Lyase Inhibition Increased Intestinal S1P, Disrupted the Intestinal Barrier and Aggravated DSS-Induced Colitis.Inflammatory bowel diseases · 2025Article
- Mesenteric adipose tissue in Crohn's disease alters the immune response of the ileal mucosa and increases angiogenesis and fibrosis.Scientific reports · 2025Article
- Antisense to human CD39 dysregulates immune metabolism in inflammatory bowel disease.Cellular & molecular immunology · 2025Article
- Adenosine-generating CD39Life science alliance · 2025Article
- Dysregulation of γδ intraepithelial lymphocytes precedes Crohn's disease-like ileitis.Science immunology · 2025Article
- SNP rs10748643 determines CD39 expression in T and NK cells through altering NFIC binding affinity rather than interfering with RNA splicing.Frontiers in immunology · 2025Article
- Article
- The transcription factor HIF-1α in NKp46+ ILCs limits chronic intestinal inflammation and fibrosis.Life science alliance · 2024Article
127 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
9 authors at 4 institutions in 2 countries.
Funding
Abstract
CD39/ENTPD1 hydrolyzes proinflammatory nucleotides to generate adenosine. As purinergic mediators have been implicated in intestinal inflammation, we hypothesized that CD39 might protect against inflammatory bowel disease. We studied these possibilities in a mouse model of colitis using mice with global CD39 deletion. We then tested whether human genetic polymorphisms in the CD39 gene might influence susceptibility to Crohn's disease. We induced colitis in mice using Dextran Sodium Sulfate (DSS). Readouts included disease activity scores, histological evidence of injury, and markers of inflammatory activity. We used HapMap cell lines to find SNPs that tag for CD39 expression, and then compared the frequency of subjects with high vs. low CD39-expression genotypes in a case-control cohort for Crohn's disease. Mice null for CD39 were highly susceptible to DSS injury, with heterozygote mice showing an intermediate phenotype compared to wild type (WT). We identified a common SNP that tags CD39 mRNA expression levels in man. The SNP tagging low levels of CD39 expression was associated with increased susceptibility to Crohn's disease in a case-control cohort comprised of 1,748 Crohn's patients and 2,936 controls (P = 0.005-0.0006). Our data indicate that CD39 deficiency exacerbates murine colitis and suggest that CD39 polymorphisms are associated with inflammatory bowel disease in humans.
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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.