ArticleThe American journal of pathology2016
IL-33 Drives Eosinophil Infiltration and Pathogenic Type 2 Helper T-Cell Immune Responses Leading to Chronic Experimental Ileitis.
Article in The American journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 74 citations in OpenAlex.
- Interleukin-33 and its receptor: multifaceted roles and emerging therapeutic potential.Nature reviews. Immunology · 2026Review
- Review
- Epithelial and stromal remodeling in murine Crohn's disease-like ileitis.bioRxiv : the preprint server for biology · 2025Article
- Unlocking IL-33: New Insights into Tumor Immunity.Immune network · 2025Review
- The angiotensin receptor blocker, losartan, reduces inflammation and fibrosis, and prevents relapse of fibrosis after steroid-induced remission, in mice prone to Crohn's disease-like ileitis.Journal of Crohn's & colitis · 2025Article
- A Diet Fortified with Anthocyanin-Rich Extract (RED) Reduces Ileal Inflammation in a Senescence-Prone Mice Model of Crohn's-Disease-like Ileitis.Antioxidants (Basel, Switzerland) · 2025Article
- Winnie Mice: A Chronic and Progressive Model of Ulcerative Colitis.Inflammatory bowel diseases · 2025Review
- Eosinophils in inflammatory bowel disease pathogenesis: an ROS-centric view.Frontiers in allergy · 2025Article
- Spatial adaptation of eosinophils and their emerging roles in homeostasis, infection and disease.Nature reviews. Immunology · 2024Review
- Article
- The Importance of Th2 Immune Responses in Mediating the Progression of Gastritis-Associated Metaplasia to Gastric Cancer.Cancers · 2024Review
- Retinoid orphan receptor gamma t (rorγt) promotes inflammatory eosinophilia but is dispensable for innate immune-mediated colitis.PloS one · 2024Article
- High-Salt-Diet (HSD) aggravates the progression of Inflammatory Bowel Disease (IBD) via regulating epithelial necroptosis.Molecular biomedicine · 2023Article
- A Deep View of the Biological Property of Interleukin-33 and Its Dysfunction in the Gut.International journal of molecular sciences · 2023Review
- Bullous pemphigoid: The role of type 2 inflammation in its pathogenesis and the prospect of targeted therapy.Frontiers in immunology · 2023Review
- Could Chronic Rhinosinusitis Increase the Risk of Ulcerative Colitis? A Nationwide Cohort Study.Diagnostics (Basel, Switzerland) · 2022Article
- Immunological mechanisms of fecal microbiota transplantation in recurrentWorld journal of gastroenterology · 2022Review
- Aging impairs arterial compliance via Klotho-mediated downregulation of B-cell population and IgG levels.Cellular and molecular life sciences : CMLS · 2022Article
- Article
- Article
Corrections and comments
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Authors and funding
18 authors at 5 institutions in 3 countries.
Funding
Abstract
Although a clear association has been established between IL-33 and inflammatory bowel disease, mechanistic studies to date, primarily using acute murine models of colitis, have yielded contradicting results, demonstrating both pathogenic and protective roles. We used a well-characterized, spontaneous model of inflammatory bowel disease [ie, SAMP1/YitFc (SAMP) mice] to investigate the role of IL-33 during chronic intestinal inflammation. Our results showed marked eosinophil infiltration into the gut mucosa with increased levels of eotaxins and type 2 helper T-cell (Th2) cytokines as disease progressed and became more severe, which could be reversed upon either eosinophil depletion or blockade of IL-33 signaling. Exogenous IL-33 administration recapitulated these effects in ilea of uninflamed (parental) control AKR/J mice. Human data supported these findings, showing colocalization and up-regulation of IL-33 and eosinophils in the colonic mucosa of inflammatory bowel disease patients versus noninflamed controls. Finally, colonization of commensal flora by fecal material transplantation into germ-free SAMP and the presence of the gut microbiome induced IL-33, subsequent eosinophil infiltration, and mounting of Th2 immune responses, leading to exacerbation of chronic intestinal inflammation characteristic of SAMP mice. These data demonstrate a pathogenic role for IL-33-mediated eosinophilia and activation of Th2 immunity in chronic intestinal inflammation that is dependent on the gut microbiome. Targeting IL-33 may represent a novel therapeutic approach to treat patients with inflammatory bowel disease.
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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.