ArticleCell2010
Virus-plus-susceptibility gene interaction determines Crohn's disease gene Atg16L1 phenotypes in intestine.
Article in Cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 524 papers, 1 of them a synthesis 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
524 citing papers in PubMed, 1 synthesis or guideline pooled it, 894 citations in OpenAlex.
- Systematic review: gastrointestinal infection and incident inflammatory bowel disease.Alimentary pharmacology & therapeutics · 2020Pooled it
- Therapy of allergic rhinitis using ribavirin spray to clear nasal commensal viruses.Signal transduction and targeted therapy · 2026Trial
- Trial
- Polymeric alpha-1 antitrypsin perturbs Paneth cell proteostasis and exacerbates intestinal inflammation.Signal transduction and targeted therapy · 2026Article
- The Interplay Between Autophagy and Porcine Epidemic Diarrhea Virus: From Molecular Mechanisms to Therapeutic Perspectives.Microorganisms · 2026Review
- Tuft cells protect against intestinal inflammation through histone deacetylase 3.Mucosal immunology · 2026Article
- OTOP2 proton channel couples luminal pH sensing to intestinal immune homeostasis.The Journal of biological chemistry · 2026Article
- Loss of Pum2 exacerbates colitis by disrupting macrophage-epithelial crosstalk and promoting epithelial necroptosis.Cell death discovery · 2026Article
- Type I and III interferons synergize with TNF to promote virally-triggered damage to the intestinal epithelium.bioRxiv : the preprint server for biology · 2026Article
- NeuroViOme: a viral orfeome collection for studies of neurodegenerative disease.Journal of neurovirology · 2026Review
- Chronic enteritis triggered by diet westernization is driven by epithelial ATG16L1-mediated autophagy.Autophagy · 2026Article
- Insufficient Expression of the Autophagic Protein ATG16L1 Results in Accelerated Carcinogenesis Related to an Aberrant B Cell Response.Cancer reports (Hoboken, N.J.) · 2026Article
- Effector-host interactome map links type III secretion systems in healthy gut microbiomes to immune modulation.Nature microbiology · 2026Article
- Filamentous bacteriophages: impact on prokaryotic virulence, eukaryotic immunity, and implications for phage therapy.Frontiers in immunology · 2026Review
- Endoplasmic reticulum stress as a mechanistic link between nutrition and inflammatory bowel disease.Frontiers in nutrition · 2026Review
- TRIM47 inhibits murine norovirus replication in a strain-dependent manner.Journal of virology · 2025Article
- Precision microbiota therapy for IBD: premise and promise.Gut microbes · 2025Review
- Genetic Convergence Analysis of CRISPR Perturbations Deciphers Gene Functional Similarity.bioRxiv : the preprint server for biology · 2025Article
- Microbiota-mediated mechanisms of mucosal immunity across the lifespan.Nature immunology · 2025Review
- Review
464 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
It is unclear why disease occurs in only a small proportion of persons carrying common risk alleles of disease susceptibility genes. Here we demonstrate that an interaction between a specific virus infection and a mutation in the Crohn's disease susceptibility gene Atg16L1 induces intestinal pathologies in mice. This virus-plus-susceptibility gene interaction generated abnormalities in granule packaging and unique patterns of gene expression in Paneth cells. Further, the response to injury induced by the toxic substance dextran sodium sulfate was fundamentally altered to include pathologies resembling aspects of Crohn's disease. These pathologies triggered by virus-plus-susceptibility gene interaction were dependent on TNFalpha and IFNgamma and were prevented by treatment with broad spectrum antibiotics. Thus, we provide a specific example of how a virus-plus-susceptibility gene interaction can, in combination with additional environmental factors and commensal bacteria, determine the phenotype of hosts carrying common risk alleles for inflammatory disease.
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What OpenQuestion holds
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.