ArticleMucosal immunology2014
Tumor necrosis factor-related apoptosis-inducing ligand mediates the resolution of allergic airway inflammation induced by chronic allergen inhalation.
Article in Mucosal immunology, 2014. 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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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- CAR-NKT Cells in Asthma: Use of NKT as a Promising Cell for CAR Therapy.Clinical reviews in allergy & immunology · 2024Review
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- TRAIL protects the immature lung from hyperoxic injury.Cell death & disease · 2022Article
- Article
- Review
- Cell Death in the Lung: The Apoptosis-Necroptosis Axis.Annual review of physiology · 2019Review
- Decreased serum TRAIL is associated with increased mortality in smokers with comorbid emphysema and coronary artery disease.Respiratory medicine · 2018Article
- Allergen Exposure in Lymphopenic Fas-Deficient Mice Results in Persistent Eosinophilia Due to Defects in Resolution of Inflammation.Frontiers in immunology · 2018Article
- Clinical perspectives of TRAIL: insights into central nervous system disorders.Cellular and molecular life sciences : CMLS · 2016Review
- Airway Inflammation after Bronchial Thermoplasty for Severe Asthma.Annals of the American Thoracic Society · 2015Observational
- Long-Term Exposure to House Dust Mite Leads to the Suppression of Allergic Airway Disease Despite Persistent Lung Inflammation.International archives of allergy and immunology · 2015Article
- Eosinophils in the lung - modulating apoptosis and efferocytosis in airway inflammation.Frontiers in immunology · 2014Review
- Intranasal administration of recombinant TRAIL down-regulates CXCL-1/KC in an ovalbumin-induced airway inflammation murine model.PloS one · 2014Article
- Switching off key signaling survival molecules to switch on the resolution of inflammation.Mediators of inflammation · 2014Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Allergic asthma can vanish over time either spontaneously or induced by allergen-specific immunotherapy. In mice with established airway allergic inflammation, chronic intranasal (IN) allergen challenges decreases progressively airway allergic inflammation. Here we compared the contribution of different regulatory pathways that could be associated with this phenomenon, known as local inhalational tolerance. We found that inhalational tolerance was not associated with increased number of regulatory T cells or suppressive cytokines. Instead, it was associated with increased apoptosis of airway inflammatory leukocytes revealed by annexin-V staining and the expression of apical caspase 8 and effector caspase 3. Also, the transition from acute to chronic phase was associated with a shift in the expression of pro-allergic to pro-apoptotic molecules. The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) was found to be a key molecule in mediating resolution of allergic inflammation because anti-TRAIL treatment blocked apoptosis and increased the infiltration of T helper type 2 (Th2) cells and eosinophils. Notably, repeated IN treatment with recombinant TRAIL in established airway allergic inflammation augmented leukocyte apoptosis and decreased the frequency of interleukin-5-producing Th2 cells and eosinophils to airways. Our data indicate that TRAIL signaling is sufficient for downmodulation of allergic airway disease, suggesting a potential therapeutic use of TRAIL for asthma treatment.
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