ArticleOncotarget2017
IL-33-induced alternatively activated macrophage attenuates the development of TNBS-induced colitis.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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.
The trial behind it
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Who cites it
26 citing papers in PubMed, 40 citations in OpenAlex.
- Interleukin-33 and its receptor: multifaceted roles and emerging therapeutic potential.Nature reviews. Immunology · 2026Review
- IL-33 promotes efferocytosis by peritoneal macrophages by a mechanism associated with rapid granulocyte IL-13 production.Frontiers in immunology · 2026Article
- Inflammation, Autoinflammation and Autoimmunity in Inflammatory Bowel Diseases.Current issues in molecular biology · 2023Review
- Distinct T helper cell-mediated antitumor immunity: T helper 2 cells in focus.Cancer pathogenesis and therapy · 2023Review
- Molecular Mechanisms Underlying IL-33-Mediated Inflammation in Inflammatory Bowel Disease.International journal of molecular sciences · 2022Review
- The IL-33-ILC2 pathway protects from amebic colitis.Mucosal immunology · 2022Article
- Immunomodulation of IL-33 and IL-37 with Vitamin D in the Neointima of Coronary Artery: A Comparative Study between Balloon Angioplasty and Stent in Hyperlipidemic Microswine.International journal of molecular sciences · 2021Article
- CD206+ macrophage is an accelerator of endometriotic-like lesion via promoting angiogenesis in the endometriosis mouse model.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
- Early Treatment of Interleukin-33 can Attenuate Lupus Development in Young NZB/W F1 Mice.Cells · 2020Article
- Low-dose curcumin reduced TNBS-associated mucin depleted foci in mice by scavenging superoxide anion and lipid peroxides, rebalancing matrix NO synthase and aconitase activities, and recoupling mitochondria.Inflammopharmacology · 2020Article
- Article
- Dual immune functions of IL-33 in inflammatory bowel disease.Histology and histopathology · 2020Review
- Mechanisms of Maintenance of Foot-and-Mouth Disease Virus Persistence Inferred From Genes Differentially Expressed in Nasopharyngeal Epithelia of Virus Carriers and Non-carriers.Frontiers in veterinary science · 2020Article
- Mucins in Intestinal Mucosal Defense and Inflammation: Learning From Clinical and Experimental Studies.Frontiers in immunology · 2020Review
- Plasma High Mobility Group Box 1 (HMGB1), Osteopontin (OPN), and Hyaluronic Acid (HA) as Admissible Biomarkers for Endometriosis.Scientific reports · 2019Article
- MicroRNA-211-5p Enhances Analgesic Effect of Dexmedetomidine on Inflammatory Visceral Pain in Rats by Suppressing ERK Signaling.Journal of molecular neuroscience : MN · 2019Article
- IL-33 Ameliorates the Development of MSU-Induced Inflammation Through Expanding MDSCs-Like Cells.Frontiers in endocrinology · 2019Article
- Divergent Roles for the IL-1 Family in Gastrointestinal Homeostasis and Inflammation.Frontiers in immunology · 2019Review
- IL-33 and IL-18 in Inflammatory Bowel Disease Etiology and Microbial Interactions.Frontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulated data have shown that alternatively activated macrophage exerts a modulatory role in many diseases, including colitis. Interleukin-33 (IL-33), a critical modulator in adaptive and innate immune, has been implicated in autoimmunity and inflammation. Previously, we have reported that IL-33 functions as a protective modulator in TNBS-induced colitis, which is closely related to a Th1-to-Th2/Treg switch. Here, we present novel evidence suggesting that IL-33 primes macrophage into alternatively activated macrophages (AAM) in TNBS-induced colitis. The strong polarized effect of IL-33 was tightly associated with the markedly increased induction of Th2-type cytokines. To confirm the beneficial effects of AAM induced by IL-33, peritoneal AAMs isolated from IL-33-treated mice were transferred to recipient mice with TNBS colitis. The adoptive transfer resulted in prominent inhibition of disease activity and inflammatory cytokines in the TNBS-treated mice. In conclusion, our data provide clear evidence that IL-33 plays a protective role in TNBS-induced colitis, which is closely related to AAM polarization.
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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.