ArticlePloS one2014
A GM-CSF/IL-33 pathway facilitates allergic airway responses to sub-threshold house dust mite exposure.
Article in PloS one, 2014. 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
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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
31 citing papers in PubMed, 65 citations in OpenAlex.
- Beneficial health effects of ultraviolet radiation: expert review and conference report.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2025Review
- Interleukin-33-activated basophils promote asthma by regulating Th2 cell entry into lung tissue.The Journal of experimental medicine · 2024Article
- Bronchial epithelial cells release inflammatory markers linked to airway inflammation and remodeling in response to TLR5 ligand flagellin.The World Allergy Organization journal · 2023Article
- Mast Cell Cytokines in Acute and Chronic Gingival Tissue Inflammation: Role of IL-33 and IL-37.International journal of molecular sciences · 2022Review
- IL-33 Enhances ACE2 Expression on Epidermal Keratinocytes in Atopic Dermatitis: A Plausible Issue for SARS-CoV-2 Transmission in Inflamed Atopic Skin.Biomedicines · 2022Article
- Understanding the development of Th2 cell-driven allergic airway disease in early life.Frontiers in allergy · 2022Review
- GM-CSF production by non-classical monocytes controls antagonistic LPS-driven functions in allergic inflammation.Cell reports · 2021Article
- IL-33 promotes innate lymphoid cell-dependent IFN-γ production required for innate immunity toeLife · 2021Article
- Regulation of Immune Responses by Nonhematopoietic Cells in Asthma.Journal of immunology (Baltimore, Md. : 1950) · 2021Review
- Inhalant Mammal-Derived Lipocalin Allergens and the Innate Immunity.Frontiers in allergy · 2021Review
- Fms-Like Tyrosine Kinase 3-Independent Dendritic Cells Are Major Mediators of Th2 Immune Responses in Allergen-Induced Asthmatic Mice.International journal of molecular sciences · 2020Article
- Imperfect storm: is interleukin-33 the Achilles heel of COVID-19?The Lancet. Rheumatology · 2020Review
- GM-CSF and IL-33 Orchestrate Polynucleation and Polyploidy of Resident Murine Alveolar Macrophages in a Murine Model of Allergic Asthma.International journal of molecular sciences · 2020Article
- GM-CSF in inflammation.The Journal of experimental medicine · 2020Review
- IL-33 Mediates Lung Inflammation by the IL-6-Type Cytokine Oncostatin M.Mediators of inflammation · 2020Article
- Epithelial cell-derived cytokines: more than just signaling the alarm.The Journal of clinical investigation · 2019Review
- A Non-canonical Pathway with Potential for Safer Modulation of Transforming Growth Factor-β1 in Steroid-Resistant Airway Diseases.iScience · 2019Article
- Endothelial cells in the innate response to allergens and initiation of atopic asthma.The Journal of clinical investigation · 2018Article
- Persistent activation of interlinked type 2 airway epithelial gene networks in sputum-derived cells from aeroallergen-sensitized symptomatic asthmatics.Scientific reports · 2018Article
- Lung epithelial cells: therapeutically inducible effectors of antimicrobial defense.Mucosal immunology · 2018Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
Allergic asthma is a chronic immune-inflammatory disease of the airways. Despite aeroallergen exposure being universal, allergic asthma affects only a fraction of individuals. This is likely related, at least in part, to the extent of allergen exposure. Regarding house dust mite (HDM), we previously identified the threshold required to elicit allergic responses in BALB/c mice. Here, we investigated the impact of an initial immune perturbation on the response to sub-threshold HDM exposure. We show that transient GM-CSF expression in the lung facilitated robust eosinophilic inflammation, long-lasting antigen-specific Th2 responses, mucus production and airway hyperresponsiveness. This was associated with increased IL-33 levels and activated CD11b(+) DCs expressing OX40L. GM-CSF-driven allergic responses were significantly blunted in IL-33-deficient mice. IL-33 was localized on alveolar type II cells and in vitro stimulation of human epithelial cells with GM-CSF enhanced intracellular IL-33 independently of IL-1α. Likewise, GM-CSF administration in vivo resulted in increased levels of IL-33 but not IL-1α. These findings suggest that exposures to environmental agents associated with GM-CSF production, including airway infections and pollutants, may decrease the threshold of allergen responsiveness and, hence, increase the susceptibility to develop allergic asthma through a GM-CSF/IL-33/OX40L pathway.
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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.