ArticleJournal of immunology (Baltimore, Md. : 1950)2017
Leukotriene C4 Potentiates IL-33-Induced Group 2 Innate Lymphoid Cell Activation and Lung Inflammation.
Article in Journal of immunology (Baltimore, Md. : 1950), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
What it found
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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.
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Who cites it
79 citing papers in PubMed, 106 citations in OpenAlex.
- Group 2 innate lymphoid cells: Where are we 15 years out?The Journal of allergy and clinical immunology · 2026Review
- Targeted metabolomic analysis of exhaled breath condensate before and after bronchial provocation by eucapnic voluntary hyperventilation in adolescents with asthma: an exploratory study.Respiratory research & clinical practice · 2026Article
- Unraveling cysteinyl leukotrienes and their receptors in inflammation through the brain-gut-lung axis.Virulence · 2025Review
- PGI2 restricts trained ILC2 responses in allergic inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- ILC2 Diversity, Location, and Function in Pulmonary Disease.Immunological reviews · 2025Review
- Tissue-Specific Metabolic Reprogramming in Innate Lymphoid Cells and Its Impact on Disease.Immune network · 2025Review
- Regulating arachidonic acid metabolism: a novel strategy to prevent colorectal inflammatory cancer transformation.Journal of Cancer · 2025Review
- Cysteinyl Leukotrienes in Allergic Inflammation.Annual review of pathology · 2025Review
- The role of ILC2s in asthma combined with atopic dermatitis: bridging the gap from research to clinical practice.Frontiers in immunology · 2025Review
- Mef2d potentiates type-2 immune responses and allergic lung inflammation.Science (New York, N.Y.) · 2024Article
- Systemic Immune Modulation by Gastrointestinal Nematodes.Annual review of immunology · 2024Review
- Implications of DNA damage in chronic lung disease.Frontiers in cell and developmental biology · 2024Review
- Genetic deficiency of the transcription factor NFAT1 confers protection against fibrogenic responses independent of immune influx.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Lower serum 15-HETE level predicts nasal ILC2 accumulation during COX-1 inhibition in AERD.The Journal of allergy and clinical immunology · 2023Article
- The Functional Role of Group 2 Innate Lymphoid Cells in Asthma.Biomolecules · 2023Review
- WFDC12-overexpressing contributes to the development of atopic dermatitis via accelerating ALOX12/15 metabolism and PAF accumulation.Cell death & disease · 2023Article
- RNA-binding protein RBM3 intrinsically suppresses lung innate lymphoid cell activation and inflammation partially through CysLT1R.Nature communications · 2022Article
- Review
- Modulating ILC2 function for treatment of type 2 airway diseases.Current trends in immunology · 2022Article
- Crosstalk between ILC2s and Th2 CD4Journal of immunology research · 2022Review
19 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Asthma is a complex disease that is promoted by dysregulated immunity and the presence of many cytokine and lipid mediators. Despite this, there is a paucity of data demonstrating the combined effects of multiple mediators in asthma pathogenesis. Group 2 innate lymphoid cells (ILC2s) have recently been shown to play important roles in the initiation of allergic inflammation; however, it is unclear whether lipid mediators, such as cysteinyl leukotrienes (CysLTs), which are present in asthma, could further amplify the effects of IL-33 on ILC2 activation and lung inflammation. In this article, we show that airway challenges with the parent CysLT, leukotriene C4 (LTC4), given in combination with low-dose IL-33 to naive wild-type mice, led to synergistic increases in airway Th2 cytokines, eosinophilia, and peribronchial inflammation compared with IL-33 alone. Further, the numbers of proliferating and cytokine-producing lung ILC2s were increased after challenge with both LTC4 and IL-33. Levels of CysLT1R, CysLT2R, and candidate leukotriene E4 receptor P2Y12 mRNAs were increased in ILC2s. The synergistic effect of LTC4 with IL-33 was completely dependent upon CysLT1R, because CysLT1R
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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.