ArticleMolecular medicine (Cambridge, Mass.)2012
Interleukin-33 ameliorates experimental colitis through promoting Th2/Foxp3⁺ regulatory T-cell responses in mice.
Article in Molecular medicine (Cambridge, Mass.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.
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Who cites it
110 citing papers in PubMed, 179 citations in OpenAlex.
- Article
- NMI Promotes Pro-Inflammatory Macrophage Polarization and Exacerbates.Inflammation · 2026Article
- IL-33 Alleviates Sepsis-Induced Liver Injury by Regulating the NF-κB/BCL-2 Pathway.Current medicinal chemistry · 2026Article
- Activity-attenuated serum albumin-fused interleukin-33 suppresses experimental autoimmune encephalomyelitis.Cell reports. Medicine · 2025Article
- Wnt/β-catenin maintains epithelial IL-33 in the colonic stem and progenitor cell niche and drives its induction in colitis.Mucosal immunology · 2025Article
- IL-33 Induces a Switch in Intestinal Metabolites Revealing the Tryptophan Pathway as a Target for Inducing Allograft Survival.Nutrients · 2024Article
- Cytokine Profile in Predicting the Effectiveness of Advanced Therapy for Ulcerative Colitis: A Narrative Review.Biomedicines · 2024Review
- A Deep View of the Biological Property of Interleukin-33 and Its Dysfunction in the Gut.International journal of molecular sciences · 2023Review
- Amphiregulin couples IL1RL1Science advances · 2023Article
- Dynamic alterations in metabolomics and transcriptomics associated with intestinal fibrosis in a 2,4,6-trinitrobenzene sulfonic acid-induced murine model.Journal of translational medicine · 2023Article
- Expression of IL-21 and IL-33 in Intestinal Mucosa of Inflammatory Bowel Disease: An Immunohistochemical Study.Diagnostics (Basel, Switzerland) · 2023Article
- CD4 T-Cell Subsets and the Pathophysiology of Inflammatory Bowel Disease.International journal of molecular sciences · 2023Review
- Effects of polyphenolic maqui (Frontiers in immunology · 2023Article
- Knowledge mapping and research trends of IL-33 from 2004 to 2022: a bibliometric analysis.Frontiers in immunology · 2023Article
- Molecular Mechanisms Underlying IL-33-Mediated Inflammation in Inflammatory Bowel Disease.International journal of molecular sciences · 2022Review
- Review
- A gut-centric view of aging: Do intestinal epithelial cells contribute to age-associated microbiota changes, inflammaging, and immunosenescence?Aging cell · 2022Review
- Free fatty acid receptor 4 deletion attenuates colitis by modulating Treg Cells via ZBED6-IL33 pathway.EBioMedicine · 2022Article
- Involvement of IL-33 in the Pathophysiology of Systemic Lupus Erythematosus: Review.International journal of molecular sciences · 2022Review
- Host-microbiota interactions shaping T-cell response and tolerance in type 1 diabetes.Frontiers in immunology · 2022Review
50 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Crohn's disease (CD) is characterized by the activation of Th1 and Th17 cells and deficiency of regulatory T cells (Tregs), leading to intestine tissue injury and destruction. As a novel cytokine of the interleukin (IL)-1 family, the role and underlying mechanisms of IL-33 in CD remain poorly understood. Here, we assess the effects and mechanisms of IL-33 on the trinitrobenzene sulfonic acid (TNBS)-induced experimental colitis that mimics human CD. We found that IL-33 levels were increased in the TNBS-treated mice, whereas recombinant IL-33 (rIL-33) administration substantially ameliorated TNBS-mediated colonic tissue injury and clinical symptoms of colitis. The protective effect of rIL-33 was partly associated with the markedly increased induction of Th2-type cytokines. Importantly, rIL-33 treatment resulted in prominently upregulated Foxp3 expression in the TNBS-treated mice, and depletion of Tregs significantly abrogated the impact of IL-33 on reducing the development of colitis. Notably, the level of CD103⁺ dendritic cells (DCs), which promotes development of Tregs, is also increased in mesenteric lymph node and lamina propria of rIL-33-treated mice. The impact of rIL-33 on CD103⁺ DC induction was the result of indirectly upregulating intestine epithelial cells that produce thymic stromal lymphopoietin and retinoic acid but do not directly act on DCs. In conclusion, our data provide clear evidence that IL-33 plays a protective role in TNBS-induced colitis, which is closely related to a Th1-to-Th2/Treg switch. Thus, IL-33 is a promising candidate for the development of new treatments for CD.
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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.