ArticleThe World Allergy Organization journal2019
Prostaglandin E2 signal inhibits T regulatory cell differentiation during allergic rhinitis inflammation through EP4 receptor.
Article in The World Allergy Organization journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Potential Roles of Prostaglandins PGD2, PGJ2, and PGE2 in the Pathogenesis of Systemic Lupus Erythematosus.International journal of molecular sciences · 2026Review
- Prostaglandin EImmunology · 2021Article
- Synergistic effect of Korean red ginseng extract and GABA mixture on the IgE production in mice via Th1/Th2 cell balance.Food science and biotechnology · 2021Article
- A TRiP Through the Roles of Transient Receptor Potential Cation Channels in Type 2 Upper Airway Inflammation.Current allergy and asthma reports · 2021Review
- Fine-Tuning the Tumour Microenvironment: Current Perspectives on the Mechanisms of Tumour Immunosuppression.Cells · 2021Review
- Contribution of Regulatory T Cell Methylation Modifications to the Pathogenesis of Allergic Airway Diseases.Journal of immunology research · 2021Review
- Non-steroidal anti-inflammatory drugs, prostaglandins, and COVID-19.British journal of pharmacology · 2020Review
- Epigenetic regulation of the PGE2 pathway modulates macrophage phenotype in normal and pathologic wound repair.JCI insight · 2020Article
- The Biology of Prostaglandins and Their Role as a Target for Allergic Airway Disease Therapy.International journal of molecular sciences · 2020Review
- Identification of Active Compounds of Mahuang Fuzi Xixin Decoction and Their Mechanisms of Action by LC-MS/MS and Network Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2020Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveAllergic rhinitis (AR) is a common disease seriously affecting quality of life, and until now the effect of medical therapy is not satisfactory. It is essential to explore in depth the pathologic mechanism of AR to offer new ideas for developing novel treatment strategies. The defect of T regulatory (Treg) cells plays a critical role in the pathogenesis of AR, but the underlying mechanism remains to be elucidated. This study aims to determine the effect of Prostaglandin E2 (PGE2) on the differentiation of Treg cells in AR patients and the involvement of E prostanoid (EP) receptor signaling pathway.
methodsThe proportion of Treg cells and the level of PGE2 in the peripheral blood of AR patients and healthy controls were compared. Differentiation rate of Treg cells under the influence of various concentrations of PGE2 with or without diverse EP receptor agonists and antagonists were investigated through cell culture and flow cytometry
resultsThe proportion of Treg cells decreased and PGE2 concentration increased in the peripheral blood of AR patients compared to healthy controls. PGE2 dose-dependently suppressed the differentiation of Treg cells from both human and mice naïve CD4
conclusionPGE2-EP4-cAMP signaling might mediate the development of AR by inhibiting the differentiation of Treg cells.
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