ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Cutting edge: Leukotriene C4 activates mouse platelets in plasma exclusively through the type 2 cysteinyl leukotriene receptor.
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 31 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
31 citing papers in PubMed, 52 citations in OpenAlex.
- Aspirin-Exacerbated Respiratory Disease Involves a Cysteinyl Leukotriene-Driven IL-33-Mediated Mast Cell Activation Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2015Trial
- Platelet-macrophage cooperation drives IL-33-dependent type 2 lung immunopathology in a sex-biased manner.The Journal of allergy and clinical immunology · 2026Article
- From Serum to Genome: γ-Glutamyltransferase Gene Family Variants Shape Ischemic Stroke Risk via Sex-Specific Gene-Environment Interactions.Life (Basel, Switzerland) · 2026Article
- Regulatory roles of bioactive lipids in vascular homeostasis and remodeling.Medical review (2021) · 2026Review
- Mast cell-specific CysLT2 receptor signaling inhibits cysteinyl leukotriene-dependent mast cell activation and type 2 allergic lung inflammation.Cell reports · 2026Article
- Platelets engage mast cells in a bilateral IL-33-driven feed-forward loop.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Profiling of lipid mediators and oxylipins in SARS-CoV-2 infection associated thrombosis.Scientific reports · 2025Article
- Development of Zafirlukast Analogues for Improved Antithrombotic Activity Through Thiol Isomerase Inhibition.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Cysteinyl Leukotrienes in Allergic Inflammation.Annual review of pathology · 2025Review
- Metabolic alterations upon SARS-CoV-2 infection and potential therapeutic targets against coronavirus infection.Signal transduction and targeted therapy · 2023Review
- Bioactive lipid regulation of platelet function, hemostasis, and thrombosis.Pharmacology & therapeutics · 2023Review
- Blockade of Platelet CysLT1R Receptor with Zafirlukast Counteracts Platelet Protumoral Action and Prevents Breast Cancer Metastasis to Bone and Lung.International journal of molecular sciences · 2022Article
- Platelets control liver tumor growth through P2Y12-dependent CD40L release in NAFLD.Cancer cell · 2022Article
- Eicosanoids in inflammation in the blood and the vessel.Frontiers in pharmacology · 2022Review
- Tuft cell-produced cysteinyl leukotrienes and IL-25 synergistically initiate lung type 2 inflammation.Science immunology · 2021Article
- Role of leukotriene pathway and montelukast in pulmonary and extrapulmonary manifestations of Covid-19: The enigmatic entity.European journal of pharmacology · 2021Review
- Leukotriene DThe Journal of allergy and clinical immunology · 2021Article
- The CysLTProceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Leukotriene Receptor Antagonist Montelukast as a Potential COVID-19 Therapeutic.Frontiers in molecular biosciences · 2020Review
- The synergistic effects of clopidogrel with montelukast may be beneficial for asthma treatment.Journal of cellular and molecular medicine · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Leukotriene C4 (LTC4) and its extracellular metabolites, LTD4 and LTE4, mediate airway inflammation. They signal through three specific receptors (type 1 cys-LT receptor [CysLT1R], CysLT2R, and GPR99) with overlapping ligand preferences. In this article, we demonstrate that LTC4, but not LTD4 or LTE4, activates mouse platelets exclusively through CysLT2R. Platelets expressed CysLT1R and CysLT2R proteins. LTC4 induced surface expression of CD62P by wild-type mouse platelets in platelet-rich plasma (PRP) and caused their secretion of thromboxane A2 and CXCL4. LTC4 was fully active on PRP from mice lacking either CysLT1R or GPR99, but completely inactive on PRP from CysLT2R-null (Cysltr2(-/-)) mice. LTC4/CysLT2R signaling required an autocrine ADP-mediated response through P2Y12 receptors. LTC4 potentiated airway inflammation in a platelet- and CysLT2R-dependent manner. Thus, CysLT2R on platelets recognizes LTC4 with unexpected selectivity. Nascent LTC4 may activate platelets at a synapse with granulocytes before it is converted to LTD4, promoting mediator generation and the formation of leukocyte-platelet complexes that facilitate inflammation.
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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.