ArticleProceedings of the National Academy of Sciences of the United States of America2018
A cytokine network involving IL-36γ, IL-23, and IL-22 promotes antimicrobial defense and recovery from intestinal barrier damage.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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
66 citing papers in PubMed, 128 citations in OpenAlex.
- Chronic Excessive Exposure to Fluoride Impairs the Intestinal Mucosal Barrier to Cause Inflammatory Response and Microbiome Dysbiosis in Rats.Biological trace element research · 2026Article
- Analysis of the use of monoclonal antibodies in the treatment of Crohn's disease.Antibody therapeutics · 2026Review
- Probing the activity of cysteine cathepsins in inflammatory bowel diseases.Scientific reports · 2025Article
- Endothelial IL-36 receptor activation promotes vascular stability to limit pathological microvessel permeability in the CNS.Cell reports · 2025Article
- Review
- Salivary shield: Rhodnius prolixus salivary glandular extract reduces intestinal immunopathology and protects against Toxoplasma gondii infection.Gut pathogens · 2025Article
- Sex-dependent modulation of acute respiratory distress syndrome byFrontiers in immunology · 2025Article
- IL-36/IL-36R signaling promotes CD4Frontiers in immunology · 2025Article
- Profiling of fecal analytes as a potential biomarker in rheumatoid arthritis.Frontiers in immunology · 2025Article
- Harnessing outer membrane vesicles derived fromFrontiers in immunology · 2025Article
- Type 17 immunity: novel insights into intestinal homeostasis and autoimmune pathogenesis driven by gut-primed T cells.Cellular & molecular immunology · 2024Review
- Development of engineered IL-36γ-hypersecreting Lactococcus lactis to improve the intestinal environment.World journal of microbiology & biotechnology · 2024Article
- IL-22 in Atopic Dermatitis.Cells · 2024Review
- Strategies for targeting cytokines in inflammatory bowel disease.Nature reviews. Immunology · 2024Review
- Innate lymphoid cells are activated in HFRS, and their function can be modulated by hantavirus-induced type I interferons.PLoS pathogens · 2024Article
- Inflammation accelerating intestinal fibrosis: from mechanism to clinic.European journal of medical research · 2024Review
- The role of Interleukin-22 in severe acute pancreatitis.Molecular medicine (Cambridge, Mass.) · 2024Review
- FloxedCells · 2024Article
- Intestinal Inflammation and Regeneration-Interdigitating Processes Controlled by Dietary Lipids in Inflammatory Bowel Disease.International journal of molecular sciences · 2024Review
- Sublingual Immunotherapy Decreased the Serum Levels of Interleukin-36Mediators of inflammation · 2024Article
6 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
10 authors at 3 institutions in 1 country.
Funding
Abstract
The gut epithelium acts to separate host immune cells from unrestricted interactions with the microbiota and other environmental stimuli. In response to epithelial damage or dysfunction, immune cells are activated to produce interleukin (IL)-22, which is involved in repair and protection of barrier surfaces. However, the specific pathways leading to IL-22 and associated antimicrobial peptide (AMP) production in response to intestinal tissue damage remain incompletely understood. Here, we define a critical IL-36/IL-23/IL-22 cytokine network that is instrumental for AMP production and host defense. Using a murine model of intestinal damage and repair, we show that IL-36γ is a potent inducer of IL-23 both in vitro and in vivo. IL-36γ-induced IL-23 required Notch2-dependent (CD11b
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.