ArticleNature communications2025
Elevated nitric oxide during colitis restrains GM-CSF production in ILC3 cells via suppressing an AhR-Cyp4f13-NF-κB axis.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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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
7 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Platelet-to-lymphocyte ratio for prognostication in immune checkpoint inhibitor-treated cancer patients: a meta-analysis of 13027 patients highlighting nivolumab-responsive renal cell carcinoma.Frontiers in immunology · 2026Pooled it
- Nitric Oxide in the Intestinal Stem Cell Niche: A Spatial Model of Nitrosative Stress and Clonal Evolution in Colitis-Associated Colorectal Cancer.Digestive diseases and sciences · 2026Review
- High-resolution promoter interaction analysis implicates genes involved in activation of type 3 innate lymphoid cells in immune disease risk.Nature genetics · 2026Article
- Review
- Identification of key bioactive compounds of medicine-food homologous substances and their multi-target intervention effects in ulcerative colitis treatment.Naunyn-Schmiedeberg's archives of pharmacology · 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
- circWWC3 enhances the progression of triple-negative breast cancer by interacting with vimentin to regulate the secretion of CSF2.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Inflammatory bowel disease (IBD) presents a significant clinical challenge, yet the way bioactive gases are implicated remains elusive. We detect elevated colonic Nos2 levels in both IBD patients and mice undergoing diverse colitis. Additionally, Nos2 deficiency significantly aggravates anti-CD40-induced colitis, along with an increase in GM-CSF production by ILC3s. We identified a previously unappreciated role of the crucial ILC3 regulator, AhR, in promoting Cyp4f13 expression to allow ILC3s to bind with externally derived nitric oxide (NO). This further restrains Cyp4f13-catalyzed ROS generation and thereby diminishes NF-κB activation strictly necessary for GM-CSF production. Accordingly, the exacerbated anti-CD40-induced colitis due to defective NO generation in Nos2 deficient mice is efficiently recovered by a Cyp4f13 inhibitor, HET0016. Importantly, IBD patients with elevated NO binding to colonic ILC3s show decreased disease activity. Thus, our findings uncover a crucial regulatory mechanism for restraining colitogenic GM-CSF production in ILC3s and underscores its implication in IBD therapy.
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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.