ArticleNature immunology2022
Group 3 innate lymphoid cells produce the growth factor HB-EGF to protect the intestine from TNF-mediated inflammation.
Article in Nature immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 81 citations in OpenAlex.
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- EPICERTIN, an engineered variant of cholera toxin B subunit, promotes survival and a pro-remodeling macrophage phenotype for mucosal healing in colitis.Mucosal immunology · 2026Article
- HBEGF/EGFR pathway activation by hUC-MSCs improves cognitive outcomes in anti-NMDAR encephalitis.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Developmentally endothelial locus-1 facilitates intestinal inflammation resolution by suppressing the Cmpk2-cGAS-STING pathway and promoting reparatory macrophage transition.Journal of advanced research · 2026Article
- From neuro-immune command circuits to microbiota-mediated regulation in the gastrointestinal tumor microenvironment.Frontiers in immunology · 2026Review
- Eosinophil-derived COX-2 protects against experimental colitis through the PGEbioRxiv : the preprint server for biology · 2025Article
- T cell KAT6A deficiency relieves inflammatory bowel disease in mice.Cell & bioscience · 2025Article
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- Regulation of innate lymphoid cell by microbial metabolites.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Protect Effects of Perilla Seed Extract and Its Active Ingredient Luteolin Against Inflammatory Bowel Disease Model via the PI3K/AKT Signal Pathway In Vivo and In Vitro.International journal of molecular sciences · 2025Article
- Comparative study of the effects of baicalin and probenecid on microRNA expression profiles in porcine aortic vascular endothelial cells infected by Glaesserella parasuis.BMC veterinary research · 2025Article
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- Enteric GABAergic neuron-derived γ-aminobutyric acid initiates expression of Igfbp7 to sustain ILC3 homeostasis.Nature immunology · 2025Article
- NRP1 instructs IL-17-producing ILC3s to drive colitis progression.Cellular & molecular immunology · 2025Article
- Biological characteristics, immune infiltration and drug prediction of PANoptosis related genes and possible regulatory mechanisms in inflammatory bowel disease.Scientific reports · 2025Article
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
Abstract
Tumor necrosis factor (TNF) drives chronic inflammation and cell death in the intestine, and blocking TNF is a therapeutic approach in inflammatory bowel disease (IBD). Despite this knowledge, the pathways that protect the intestine from TNF are incompletely understood. Here we demonstrate that group 3 innate lymphoid cells (ILC3s) protect the intestinal epithelium from TNF-induced cell death. This occurs independent of interleukin-22 (IL-22), and we identify that ILC3s are a dominant source of heparin-binding epidermal growth factor-like growth factor (HB-EGF). ILC3s produce HB-EGF in response to prostaglandin E2 (PGE2) and engagement of the EP2 receptor. Mice lacking ILC3-derived HB-EGF exhibit increased susceptibility to TNF-mediated epithelial cell death and experimental intestinal inflammation. Finally, human ILC3s produce HB-EGF and are reduced from the inflamed intestine. These results define an essential role for ILC3-derived HB-EGF in protecting the intestine from TNF and indicate that disruption of this pathway contributes to IBD.
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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.