ArticleJournal of gastroenterology2012
Blocking IL-25 signalling protects against gut inflammation in a type-2 model of colitis by suppressing nuocyte and NKT derived IL-13.
Article in Journal of gastroenterology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 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
81 citing papers in PubMed, 128 citations in OpenAlex.
- Tuft cells protect against intestinal inflammation through histone deacetylase 3.Mucosal immunology · 2026Article
- Tuft-cell-derived IL-25 regulates intestinal ILC2 in response toFrontiers in immunology · 2026Article
- Global Research Trends in Innate Lymphoid Cells in the Gut and Kidney: A Bibliometric and Visual Analysis.Endocrine, metabolic & immune disorders drug targets · 2026Review
- CD28 and ICOS in immune regulation: Structural insights and therapeutic targeting.Bioorganic & medicinal chemistry letters · 2025Review
- Retinoic Acid Modulates Immune Differentiation in a Human Small Intestinal In Vitro Model.Cells · 2025Article
- Tuft cell IL-17RB restrains IL-25 bioavailability and reveals context-dependent ILC2 hypoproliferation.Nature immunology · 2025Article
- Unraveling the complexity of ulcerative colitis: insights into cytokine dysregulation and targeted therapies.EXCLI journal · 2025Review
- Fundamental and emerging insights into innate and adaptive immunity in inflammatory bowel diseases.Frontiers in immunology · 2025Review
- The role of the tuft cell-interleukin-25 axis in the pathogenesis of inflammatory bowel disease.Frontiers in immunology · 2025Review
- Immunological and cytokine profile (IL-25 and IL-35) in patients withArchives of Razi Institute · 2024Article
- Innate Type-2 Cytokines: From Immune Regulation to Therapeutic Targets.Immune network · 2024Review
- Disease pathogenesis and barrier functions regulated by group 3 innate lymphoid cells.Seminars in immunopathology · 2024Review
- Dissecting Innate and Adaptive Immunity in Inflammatory Bowel Disease: Immune Compartmentalization, Microbiota Crosstalk, and Emerging Therapies.Journal of inflammation research · 2024Review
- Based on Weighted Gene Co-Expression Network Analysis Reveals the Hub Immune Infiltration-Related Genes Associated with Ulcerative Colitis.Journal of inflammation research · 2024Article
- Innate lymphoid cells and innate-like T cells in cancer - at the crossroads of innate and adaptive immunity.Nature reviews. Cancer · 2023Review
- Development of Adaptive Immunity and Its Role in Lung Remodeling.Advances in experimental medicine and biology · 2023Article
- Role of CD1d and iNKT cells in regulating intestinal inflammation.Frontiers in immunology · 2023Review
- TSLP, IL-33, and IL-25: Not just for allergy and helminth infection.The Journal of allergy and clinical immunology · 2022Review
- Discovery and multi-parametric optimization of a high-affinity antibody against interleukin-25 with neutralizing activity in a mouse model of skin inflammation.Antibody therapeutics · 2022Article
- Inflammatory Bowel Disease: A Review of Pre-Clinical Murine Models of Human Disease.International journal of molecular sciences · 2022Review
21 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
11 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundInterleukin-25 (IL-25) is a potent activator of type-2 immune responses. Mucosal inflammation in ulcerative colitis is driven by type-2 cytokines. We have previously shown that a neutralizing anti-IL-25 antibody abrogated airways hyperreactivity in an experimental model of lung allergy. Therefore, we asked whether blocking IL-25 via neutralizing antibodies against the ligand or its receptor IL-17BR could protect against inflammation in an oxazolone-induced mouse model of colitis.
methodsNeutralizing antibodies to IL-25 or IL-17BR were administered to mice with oxazolone-induced colitis, a model of ulcerative colitis. The disease onset was evaluated by weight loss and degree of colon ulceration. Also, lamina propria and mesenteric lymph node (MLN) infiltrates were assessed for mucosal inflammation and cultured in vitro to determine cytokine production.
resultsWe found that in oxazolone colitis IL-25 production derives from intestinal epithelial cells and that IL-17BR(+) IL-13-producing natural killer T (NKT) cells and nuocytes drive the intestinal inflammation. Blocking IL-25 signalling considerably improved the clinical aspects of the disease, including weight loss and colon ulceration, and resulted in fewer nuocytes and NKT cells infiltrating the mucosa. The improved pathology correlated with a decrease in IL-13 production by lamina propria cells, a decrease in the production of other type-2 cytokines by MLN cells, and a decrease in blood eosinophilia and IgE.
conclusionIL-25 plays a pro-inflammatory role in the oxazolone colitis model, and neutralizing antibodies to IL-25 or IL-17BR can slow the ongoing inflammation in this disease. Because this model mimics aspects of human ulcerative colitis, these antibodies may represent potential therapeutics for reducing gut inflammation in patients.
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.