ArticleJournal of immunology (Baltimore, Md. : 1950)2013
IL-33 induces a hyporesponsive phenotype in human and mouse mast cells.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The trial behind it
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Who cites it
32 citing papers in PubMed, 65 citations in OpenAlex.
- The IL-33-PIN1-IRAK-M axis is critical for type 2 immunity in IL-33-induced allergic airway inflammation.Nature communications · 2018Trial
- Dual role of IFNγ in reprogramming the undifferentiated pleomorphic sarcoma cell line JBT19 towards cytotoxic chemotherapy and antitumor immunity.Oncology letters · 2026Article
- Article
- Regulation of Airway Epithelial-Derived Alarmins in Asthma: Perspectives for Therapeutic Targets.Biomedicines · 2024Review
- IL-33 potentiates histaminergic itch.The Journal of allergy and clinical immunology · 2024Article
- Review
- Article
- SCF and IL-33 regulate mouse mast cell phenotypic and functional plasticity supporting a pro-inflammatory microenvironment.Cell death & disease · 2023Article
- Review
- LL-37 as a Powerful Molecular Tool for Boosting the Performance of Ex Vivo-Produced Human Dendritic Cells for Cancer Immunotherapy.Pharmaceutics · 2022Article
- IL-33 Induces an Antiviral Signature in Mast Cells but Enhances Their Permissiveness for Human Rhinovirus Infection.Viruses · 2022Article
- Mast Cells and Dendritic Cells as Cellular Immune Checkpoints in Immunotherapy of Solid Tumors.International journal of molecular sciences · 2022Review
- The Role of TGFβ and Other Cytokines in Regulating Mast Cell Functions in Allergic Inflammation.International journal of molecular sciences · 2022Review
- Review
- The innate face of Giant Cell Arteritis: Insight into cellular and molecular innate immunity pathways to unravel new possible biomarkers of disease.Frontiers in molecular medicine · 2022Review
- Review
- Novel Approaches in the Inhibition of IgE-Induced Mast Cell Reactivity in Food Allergy.Frontiers in immunology · 2021Review
- Epigenetic programming underpins B-cell dysfunction in peanut and multi-food allergy.Clinical & translational immunology · 2021Article
- Acute Conditioning of Antigen-Expanded CD8Cancers · 2020Article
- Resveratrol inhibits IL-33-mediated mast cell activation by targeting the MK2/3-PI3K/Akt axis.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 2 countries.
Funding
Abstract
IL-33 is elevated in afflicted tissues of patients with mast cell (MC)-dependent chronic allergic diseases. Based on its acute effects on mouse MCs, IL-33 is thought to play a role in the pathogenesis of allergic disease through MC activation. However, the manifestations of prolonged IL-33 exposure on human MC function, which best reflect the conditions associated with chronic allergic disease, are unknown. In this study, we found that long-term exposure of human and mouse MCs to IL-33 results in a substantial reduction of MC activation in response to Ag. This reduction required >72 h exposure to IL-33 for onset and 1-2 wk for reversion following IL-33 removal. This hyporesponsive phenotype was determined to be a consequence of MyD88-dependent attenuation of signaling processes necessary for MC activation, including Ag-mediated calcium mobilization and cytoskeletal reorganization, potentially as a consequence of downregulation of the expression of phospholipase Cγ(1) and Hck. These findings suggest that IL-33 may play a protective, rather than a causative, role in MC activation under chronic conditions and, furthermore, reveal regulated plasticity in the MC activation phenotype. The ability to downregulate MC activation in this manner may provide alternative approaches for treatment of MC-driven disease.
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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.