ReviewCell death & disease2019
ILC3 function as a double-edged sword in inflammatory bowel diseases.
Review in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 163 papers.
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
163 citing papers in PubMed, 254 citations in OpenAlex.
- ILC3s as central regulators of mucosal homeostasis and disease pathogenesis (Review).International journal of molecular medicine · 2026Review
- Review
- Article
- High-resolution promoter interaction analysis implicates genes involved in activation of type 3 innate lymphoid cells in immune disease risk.Nature genetics · 2026Article
- Article
- Urolithin A activates aryl hydrocarbon receptor-NLRP6-mediated pathways in intestinal epithelial cells to modulate mucosal immunity and strengthen gut barrier integrity.Nature communications · 2026Article
- Regulation of antiviral immunity by PD-1 during respiratory syncitial virus infection and upon vaccination.iScience · 2026Article
- Review
- Nerves Stimulate Cross-talk Between Gastric Cancer and Group 3 Innate Lymphoid Cells to Enhance Immunosuppression.Cancer research · 2026Article
- Effect of the intestinal microbiota on TSeminars in immunopathology · 2026Review
- Disturbed LTB4 Metabolism in ILC2s Aggravates Ulcerative Colitis via Intercellular ATP Accumulation.Inflammation · 2026Article
- Methanobrevibacter smithii activates immune microenvironment of intestinum tenue in a mouse model.Archives of microbiology · 2026Article
- Leukemia-driven expansion of type 3 innate lymphoid cell facilitates a pro-tumoral microenvironment in acute myeloid leukemia.Leukemia · 2026Article
- High-resolution promoter interaction analysis implicates genes involved in the activation of Type 3 Innate Lymphoid Cells in autoimmune disease risk.bioRxiv : the preprint server for biology · 2026Article
- Unraveling the pleiotropic roles of the mTOR-glycolytic axis in ulcerative colitis: from immunometabolic dysregulation to mucosal barrier remodeling.Frontiers in immunology · 2026Review
- ILC imbalance - a new piece in the gut-kidney axis puzzle.Frontiers in immunology · 2026Review
- Bidirectional Crosstalk Between Intestinal Epithelium and Immune Microenvironment in Inflammatory Bowel Disease: Mechanisms and Therapeutic Implications.Journal of inflammation research · 2026Review
- Aryl hydrocarbon receptor: a potential target for natural products in the treatment of inflammatory bowel disease.Frontiers in immunology · 2026Review
- Identification, characterization, and expansion of innate lymphoid cells derived from canine peripheral blood mononuclear cells.Frontiers in immunology · 2026Article
- The shifting balance: innate lymphoid cell plasticity in chronic gut diseases.Frontiers in immunology · 2026Review
103 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
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory bowel diseases (IBD), composed mainly of Crohn's disease (CD) and ulcerative colitis (UC), are strongly implicated in the development of intestinal inflammation lesions. Its exact etiology and pathogenesis are still undetermined. Recently accumulating evidence supports that group 3 innate lymphoid cells (ILC3) are responsible for gastrointestinal mucosal homeostasis through moderate generation of IL-22, IL-17, and GM-CSF in the physiological state. ILC3 contribute to the progression and aggravation of IBD while both IL-22 and IL-17, along with IFN-γ, are overexpressed by the dysregulation of NCR
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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.