ArticleNature communications2023
Interleukin 31 receptor α promotes smooth muscle cell contraction and airway hyperresponsiveness in asthma.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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
14 citing papers in PubMed, 15 citations in OpenAlex.
- Roles of Interleukin-31 in Allergen-Driven Cough: Linking Protease-Activated Receptor-2 Activation and Vagal Ganglion Sensitization in a Dermatophagoides farinae-Induced Asthma Model.Brain and behavior · 2026Article
- HuR Regulates GATA3-Driven Type 2 Inflammation in CD4bioRxiv : the preprint server for biology · 2026Article
- PLK1 inhibition by volasertib suppresses key transcriptional regulators underlying fibroblast activation and pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Elucidating molecular mechanisms of allergic sensitization to olive pollen through transcriptomics.Frontiers in immunology · 2026Article
- Yanghe Pingchuan granules inhibit cellular senescence in airway smooth muscle cells to improve bronchial asthma via modulating Nrf2 acetylation.Respiratory research · 2025Article
- Geometrically controlled cardiac microtissues promote vascularization and reduce inflammationCell biomaterials · 2025Article
- SERPINB10 promotes macrophage M2 polarization and airway inflammation in asthma.Respiratory research · 2025Article
- Review
- Emerging Concepts in Cytokine Regulation of Airway Remodeling in Asthma.Immunological reviews · 2025Review
- T1-T2 Interplay in the Complex Immune Landscape of Severe Asthma.Immunological reviews · 2025Review
- Causal Association Between 12 Micronutrients and Common Chronic Respiratory Diseases: A Bidirectional Two-Sample Mendelian Randomization Study.Genetics research · 2025Article
- Interleukin-31 in Respiratory Type 2 Inflammatory Diseases: Mechanistic Insights and Therapeutic Potential.Journal of inflammation research · 2025Review
- Kiss1 receptor knockout exacerbates airway hyperresponsiveness and remodeling in a mouse model of allergic asthma.Respiratory research · 2024Article
- The IL-33/IL-31 Axis in Allergic and Immune-Mediated Diseases.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Asthma is a chronic inflammatory airway disease characterized by airway hyperresponsiveness (AHR), inflammation, and goblet cell hyperplasia. Multiple cytokines, including IFNγ, IL-4, and IL-13 are associated with asthma; however, the mechanisms underlying the effects of these cytokines remain unclear. Here, we report a significant increase in the expression of IL-31RA, but not its cognate ligand IL-31, in mouse models of allergic asthma. In support of this, IFNγ, IL-4, and IL-13 upregulated IL-31RA but not IL-31 in both human and mice primary airway smooth muscle cells (ASMC) isolated from the airways of murine and human lungs. Importantly, the loss of IL-31RA attenuated AHR but had no effect on inflammation and goblet cell hyperplasia in mice challenged with allergens or treated with IL-13 or IFNγ. We show that IL-31RA functions as a positive regulator of muscarinic acetylcholine receptor 3 expression, augmenting calcium levels and myosin light chain phosphorylation in human and murine ASMC. These findings identify a role for IL-31RA in AHR that is distinct from airway inflammation and goblet cell hyperplasia in asthma.
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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.