ArticlePloS one2020
Allergic inflammation is initiated by IL-33-dependent crosstalk between mast cells and basophils.
Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 31 citations in OpenAlex.
- Microporous annealed particle scaffolds avoid foreign body response by down regulating complement-fibroblast-macrophage signaling loop.bioRxiv : the preprint server for biology · 2026Article
- Mechanistic Insights into Flavonoids in Cosmetic Applications: Multifunctional Roles and Formulation Considerations.Clinical, cosmetic and investigational dermatology · 2026Review
- NADPH oxidase 1-PKCδ-dependent ZO-1 phosphorylation mediates IL-33-induced inner blood-retinal barrier disruption in proliferative retinopathies.American journal of physiology. Cell physiology · 2025Article
- Unlocking IL-33: New Insights into Tumor Immunity.Immune network · 2025Review
- IL-33 signaling is dispensable for the IL-10-induced enhancement of mast cell responses during food allergy.Frontiers in immunology · 2025Article
- MrgprA3 neurons drive cutaneous immunity against helminths through selective control of myeloid-derived IL-33.Nature immunology · 2024Article
- Conjugation of IL-33 to Microporous Annealed Particle Scaffolds Enhances Type 2-Like Immune Responses In Vitro and In Vivo.Advanced healthcare materials · 2024Article
- Cancer stem cells release interleukin-33 within large oncosomes to promote immunosuppressive differentiation of macrophage precursors.Immunity · 2024Article
- A neutrophil elastase-generated mature form of IL-33 is a potent regulator of endothelial cell activation and proliferative retinopathy.Experimental & molecular medicine · 2024Article
- IL-10 Differentially Promotes Mast Cell Responsiveness to IL-33, Resulting in Enhancement of Type 2 Inflammation and Suppression of Neutrophilia.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Neferine Attenuates HDM-Induced Allergic Inflammation by Inhibiting the Activation of Dendritic Cell.Inflammation · 2023Article
- Vascular cell-adhesion molecule 1 (VCAM-1) regulates JunB-mediated IL-8/CXCL1 expression and pathological neovascularization.Communications biology · 2023Article
- Potential Role of Innate Lymphoid Cells in the Pathogenesis and Treatment of Skin Diseases.Journal of clinical medicine · 2023Review
- Article
- Promoting New Approach Methodologies (NAMs) for research on skin color changes in response to environmental stress factors: tobacco and air pollution.Frontiers in toxicology · 2023Review
- Mast Cell Cytokines in Acute and Chronic Gingival Tissue Inflammation: Role of IL-33 and IL-37.International journal of molecular sciences · 2022Review
- IL-33 enhances Jagged1 mediated NOTCH1 intracellular domain (NICD) deubiquitination and pathological angiogenesis in proliferative retinopathy.Communications biology · 2022Article
- Different Phenotypes in Asthma: Clinical Findings and Experimental Animal Models.Clinical reviews in allergy & immunology · 2022Review
- Differential Effects of Alarmins on Human and Mouse Basophils.Frontiers in immunology · 2022Article
- Basophils from allergy to cancer.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
IgE-primed mast cells in peripheral tissues, including the skin, lung, and intestine, are key initiators of allergen-triggered edema and inflammation. Particularly in severe forms of allergy, this inflammation becomes strongly neutrophil dominated, and yet how mast cells coordinate this type of response is unknown. We and others have reported that activated mast cells--a hematopoietic cell type--can produce IL-33, a cytokine known to participate in allergic responses but generally considered as being of epithelial origin and driving Type 2 immune responses (e.g., ILC2 and eosinophil activation). Using models of skin anaphylaxis, our data reveal that mast cell-derived IL-33 also initiates neutrophilic inflammation. We demonstrate a cellular crosstalk mechanism whereby activated mast cells crosstalk to IL-33 receptor-bearing basophils, driving these basophils to adopt a unique response signature rich in neutrophil-associated molecules. We further establish that basophil expression of CXCL1 is necessary for IgE-driven neutrophilic inflammation. Our findings thus unearth a new mechanism by which mast cells initiate local inflammation after antigen triggering and might explain the complex inflammatory phenotypes observed in severe allergic diseases. Moreover, our findings (i) establish a functional link from IL-33 to neutrophilic inflammation that extends IL-33-mediated biology well beyond that of Type 2 immunity, and (ii) demonstrate the functional importance of hematopoietic cell-derived IL-33 in allergic pathogenesis.
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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.