ArticleCell cycle (Georgetown, Tex.)2020
Epithelial cells expressed IL-33 to promote degranulation of mast cells through inhibition on ST2/PI3K/mTOR-mediated autophagy in allergic rhinitis.
Article in Cell cycle (Georgetown, Tex.), 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, 46 citations in OpenAlex.
- Quercetin modulates mast cell activation and the IL-33/ST2/NF-κB axis in allergic rhinitis.Scientific reports · 2026Article
- The role of nasal microbiota and type 2 innate lymphoid cells in the pathogenesis of allergic rhinitis.Biochemistry and biophysics reports · 2026Article
- Analysis and validation of diagnostic biomarkers and immune cell infiltration characteristics in chronic spontaneous urticaria and autophagy based on machine learning.The World Allergy Organization journal · 2026Article
- The IL-33/ST2 Axis Promotes Traumatic Heterotopic Ossification by Driving Macrophage and Mast Cell-Mediated Inflammation via Autophagy Defects.International journal of biological sciences · 2026Article
- The Immunogenetic Landscape of Allergic Rhinitis: from Cellular Effectors to Gene Regulation and Targeted Therapies.International journal of biological sciences · 2026Review
- Autophagy and mitophagy in dermatological disease: a comprehensive review from molecular pathways to therapeutic frontiers.Biology direct · 2025Review
- Interleukin 33 Promotes Liver Sinusoidal Endothelial Cell Dysfunction and Hepatic Fibrosis in Diabetic Mice.Diabetes & metabolism journal · 2025Article
- Crosstalk Between Allergic Inflammation and Autophagy.International journal of molecular sciences · 2025Review
- Inhibition of dendritic cell autophagy alleviates the progression of allergic rhinitis by inhibiting Th1/Th2/Th17 immune imbalance and inflammation.Histology and histopathology · 2025Article
- Potential Mechanisms of Traditional Chinese Medicine for the Treatment of Allergic Rhinitis: Evidence from Molecular and Clinical Studies.International journal of general medicine · 2025Review
- Exploring the Therapeutic Role of Natural Products in Allergic Rhinitis Based on Pathophysiology and Signaling Pathways.Journal of asthma and allergy · 2025Review
- Exploring Advances in Natural Plant Molecules for Allergic Rhinitis Immunomodulation in Vivo and in Vitro.International journal of general medicine · 2025Review
- Integrated gut microbiome and metabolomics analysis reveals microbial-metabolic cross-talk in allergic rhinitis.Frontiers in microbiology · 2025Article
- Article
- Review
- Regulatory Functions of Hypoxia in Host-Parasite Interactions: A Focus on Enteric, Tissue, and Blood Protozoa.Microorganisms · 2023Review
- IL-33/ST2 antagonizes STING signal transduction via autophagy in response to acetaminophen-mediated toxicological immunity.Cell communication and signaling : CCS · 2023Article
- Pathogenesis of allergic diseases and implications for therapeutic interventions.Signal transduction and targeted therapy · 2023Review
- New insights into autophagy in inflammatory subtypes of asthma.Frontiers in immunology · 2023Review
- IL-33 mediates Pseudomonas induced airway fibrogenesis and is associated with CLAD.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2023Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nasal epithelial cells are the first barrier against allergen infiltration in allergic rhinitis (AR), and the relationship between nasal epithelial cells and mast cell-mediated hypersensitivity remains unclear. This study aimed to investigate the possible association between allergen-challenged nasal epithelial cells (AR-HNEpC) and mast cell degranulation in AR. Our data revealed that calcium influx and degranulation were increased in AR-HNEpC-co-cultured mast cells. Expression of IL-33, a factor that binds to ST2 receptors on mast cells and regulates their degranulation, was elevated in AR-HNEpC. Blocking IL-33/ST2 pathway activated autophagy and inhibited degranulation and inflammatory factor release in mast cells. Furthermore, PI3K/mTOR was increased in IL-33-treated mast cells. Inhibition on PI3K/mTOR pathway enhanced autophagy and inhibited degranulation. Analysis using an
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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.