ArticleAllergy2023
Metabolic regulation by prostaglandin E
Article in Allergy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 18 citations in OpenAlex.
- The update of prostaglandin E2 receptor subtype 4 (EP4) in inflammatory diseases.Genes & diseases · 2026Review
- Adipocyte-derived LTB4 programs human NKG2AJournal for immunotherapy of cancer · 2026Article
- Review
- Glycolytic reprogramming in cancer: immune crosstalk, nutrient competition, and supportive care perspectives.Frontiers in immunology · 2026Review
- The Major Role of Type 2 Inflammation in Asthma: From the Perspective of Immunological Mechanism.BioMed research international · 2026Review
- Glycolytic reprogramming and cell-specific lactylation in asthma: an evidence-graded framework for testable metabolic-epigenetic profiles.Frontiers in immunology · 2026Review
- Integrated Transcriptomic and Metabolomic Analysis Reveals Regulatory Effects of Fermented Chinese Chive on Early Testicular Development in Piglets.Antioxidants (Basel, Switzerland) · 2025Article
- Potential of interleukin-7 in sepsis as a biomarker and therapeutic agent: a narrative review.Frontiers in medicine · 2025Review
- The role of ILC2s in asthma combined with atopic dermatitis: bridging the gap from research to clinical practice.Frontiers in immunology · 2025Review
- Research Progress on Glycolysis in the Pathogenesis of Asthma.Journal of asthma and allergy · 2025Review
- Low Prostaglandin EJournal of clinical medicine · 2024Review
- Metabolic adaptations of ILC2 and Th2 cells in type 2 immunity.Current opinion in immunology · 2024Review
- RGS4 controls airway hyperresponsiveness through GAP-independent mechanisms.The Journal of biological chemistry · 2024Article
- The modulation of pulmonary group 2 innate lymphoid cell function in asthma: from inflammatory mediators to environmental and metabolic factors.Experimental & molecular medicine · 2023Review
- Metabolic regulation by prostaglandin EAllergy · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 6 institutions in 4 countries.
Funding
Abstract
backgroundGroup 2 innate lymphoid cells (ILC2s) play a critical role in asthma pathogenesis. Non-steroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (NERD) is associated with reduced signaling via EP2, a receptor for prostaglandin E
methodsThe roles of PGE
resultsDeficiency of EP2 rather than EP4 augments IL-33-induced mouse lung ILC2 responses and eosinophilic inflammation in vivo. In contrast, exogenous agonism of EP4 and EP2 or inhibition of phosphodiesterase markedly restricts IL-33-induced lung ILC2 responses. Mechanistically, PGE
conclusionWe have defined a mechanism for optimal suppression of mouse lung ILC2 responses by endogenous PGE
Indexed as
Identifiers
What OpenQuestion holds
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.