ArticleJournal of immunology research2018
IL-33 Protects Mice against DSS-Induced Chronic Colitis by Increasing Both Regulatory B Cell and Regulatory T Cell Responses as Well as Decreasing Th17 Cell Response.
Article in Journal of immunology research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Activity-attenuated serum albumin-fused interleukin-33 suppresses experimental autoimmune encephalomyelitis.Cell reports. Medicine · 2025Article
- Extracellular vesicles produced by bone marrow mesenchymal stem cells overexpressing programmed death-ligand 1 ameliorate dextran sodium sulfate-induced ulcerative colitis in rats by regulating Th17/Treg cell balance through PTEN/PI3K/AKT/mTOR axis.Journal of gastroenterology and hepatology · 2022Article
- [WDSUB1 knockdown alleviates dextran sulfate sodium-induced colitis in mice by inhibiting nuclear factor-κB signaling pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Mesenchymal (Stem) Stromal Cells Based as New Therapeutic Alternative in Inflammatory Bowel Disease: Basic Mechanisms, Experimental and Clinical Evidence, and Challenges.International journal of molecular sciences · 2022Review
- Maternal prebiotic supplementation impacts colitis development in offspring mice.Frontiers in nutrition · 2022Article
- Interleukin-33 signaling exacerbates experimental infectious colitis by enhancing gut permeability and inhibiting protective Th17 immunity.Mucosal immunology · 2021Article
- IL-33 is produced by colon fibroblasts and differentially regulated in acute and chronic murine colitis.Scientific reports · 2021Article
- IL-33 Drives Expansion of Type 2 Innate Lymphoid Cells and Regulatory T Cells and Protects Mice From Severe, Acute Colitis.Frontiers in immunology · 2021Article
- Advances of Regulatory B Cells in Autoimmune Diseases.Frontiers in immunology · 2021Review
- IL-33/ST2 Axis Deficiency Exacerbates Hepatic Pathology by Regulating Treg and Th17 Cells in Murine Schistosomiasis Japonica.Journal of inflammation research · 2021Article
- Early Treatment of Interleukin-33 can Attenuate Lupus Development in Young NZB/W F1 Mice.Cells · 2020Article
- Role of Interleukin-33 inFrontiers in immunology · 2020Article
- Paradoxical role of Breg-inducing cytokines in autoimmune diseases.Journal of translational autoimmunity · 2019Review
- Inhibition of miR-378a-3p by Inflammation Enhances IL-33 Levels: A Novel Mechanism of Alarmin Modulation in Ulcerative Colitis.Frontiers in immunology · 2019Article
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12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPreviously, we have reported that IL-33 functioned as a protective modulator in dextran sulfate sodium- (DSS-) induced chronic colitis by suppressing Th17 cell response in colon lamina propria and IL-33 induced both regulatory B cells (Bregs) and regulatory T cells (Tregs) in mesenteric lymph nodes (MLNs) of mice with DSS-induced acute colitis. Moreover, we speculated that IL-33 would promote the Treg or Breg responses leading to the attenuation of DSS-induced chronic colitis. So, we investigated the role of IL-33 on Bregs and Tregs in the MLN of DSS-induced chronic colitis mice.
methodsIL-33 was administered by intraperitoneal injection to mice with DSS-induced chronic colitis. Clinical symptoms, colon length, and histological changes were determined. The production of cytokines was measured by ELISA. The T and B cell subsets were measured by flow cytometry. The expression of mRNA of transcription factors was measured by quantitative real-time PCR.
resultsWe show that IL-33 treatment increases both Breg and Treg responses in the MLN of mice with DSS-induced chronic colitis. Moreover, IL-33 treatment also decreases Th17 cell response in the MLN of mice with DSS-induced chronic colitis.
conclusionOur data provide clear evidence that IL-33 plays a protective role in DSS-induced chronic colitis, which is closely related to increasing Breg and Treg responses in the MLN of mice as well as suppressing Th17 cell responses.
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