ArticleJournal of immunology (Baltimore, Md. : 1950)2017
IL-18 Drives ILC3 Proliferation and Promotes IL-22 Production via NF-κB.
Article in Journal of immunology (Baltimore, Md. : 1950), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
60 citing papers in PubMed, 95 citations in OpenAlex.
- IL-22 promotes the establishment of chronic gammaherpesvirus infection by supporting the germinal center response.PLoS pathogens · 2026Article
- Peyer's patch M cells organize an epithelial niche that sustains group 3 innate lymphoid cells and IL-22.Nature immunology · 2026Article
- 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
- Gasdermins against intracellular bacterial pathogens.Nature microbiology · 2026Review
- Innate lymphoid cell heterogeneity and etiology-specific reprogramming in hepatocellular carcinoma.NPJ precision oncology · 2026Article
- Assessment of Serum Interleukins 18 and 22 in Predicting Neonatal Sepsis and Mortality: A Case-Control Study.Clinical medicine insights. Pediatrics · 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
- T helper 17 cells and group 3 innate lymphoid cells define a spectrum of psoriasis endotypes.Frontiers in immunology · 2026Review
- mtROS-NF-κB signaling supports ILC3 function and survival during sepsis-induced intestinal injury.Frontiers in immunology · 2026Article
- Programmed cell death in triple-negative breast cancer.Cellular & molecular biology letters · 2025Review
- Enteric tuft cell inflammasome activation drives NKp46+ILC3 IL22 via PGD2 and inhibits Salmonella.The Journal of experimental medicine · 2025Article
- A vasculature-resident innate lymphoid cell population in mouse lungs.Nature communications · 2025Article
- Targeting highly attenuated IL-18 to PD-1 for enhanced anti-tumor activity.Frontiers in immunology · 2025Article
- A multi-omics approach to overeating and inactivity-induced muscle atrophy in db/db mice.Journal of cachexia, sarcopenia and muscle · 2024Article
- Identification of a genetic region linked to tolerance to MRSA infection using Collaborative Cross mice.PLoS genetics · 2024Article
- LSD1 drives intestinal epithelial maturation and controls small intestinal immune cell composition independent of microbiota in a murine model.Nature communications · 2024Article
- Epithelial regulation of microbiota-immune cell dynamics.Mucosal immunology · 2024Review
- Article
- Understanding Type 3 Innate Lymphoid Cells and Crosstalk with the Microbiota: A Skin Connection.International journal of molecular sciences · 2024Review
- Activation of ILC2s through constitutive IFNγ signaling reduction leads to spontaneous pulmonary fibrosis.Nature communications · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors at 2 institutions in 1 country.
Funding
Abstract
Group 3 innate lymphoid cells (ILC3s) are important regulators of the immune system, maintaining homeostasis in the presence of commensal bacteria, but activating immune defenses in response to microbial pathogens. ILC3s are a robust source of IL-22, a cytokine critical for stimulating the antimicrobial response. We sought to identify cytokines that can promote proliferation and induce or maintain IL-22 production by ILC3s and determine a molecular mechanism for this process. We identified IL-18 as a cytokine that cooperates with an ILC3 survival factor, IL-15, to induce proliferation of human ILC3s, as well as induce and maintain IL-22 production. To determine a mechanism of action, we examined the NF-κB pathway, which is activated by IL-18 signaling. We found that the NF-κB complex signaling component, p65, binds to the proximal region of the
Indexed as
Identifiers
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.