ArticlePloS one2014
γδ T cells are required for pulmonary IL-17A expression after ozone exposure in mice: role of TNFα.
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 22 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
22 citing papers in PubMed, 29 citations in OpenAlex.
- Uncovering the mysteries of human gamma delta T cells: from origins to novel therapeutics.Frontiers in immunology · 2025Review
- Inconsequential role for chemerin-like receptor 1 in the manifestation of ozone-induced lung pathophysiology in male mice.Physiological reports · 2024Article
- Article
- "Air That Once Was Breath" Part 1: Wildfire-Smoke-Induced Mechanisms of Airway Inflammation - "Climate Change, Allergy and Immunology" Special IAAI Article Collection: Collegium Internationale Allergologicum Update 2023.International archives of allergy and immunology · 2024Review
- Interleukin-11 receptor subunit α-1 is required for maximal airway responsiveness to methacholine after acute exposure to ozone.American journal of physiology. Regulatory, integrative and comparative physiology · 2022Article
- Hypoxia pretreatment enhances the therapeutic potential of mesenchymal stem cells (BMSCs) on ozone-induced lung injury in rats.Cell and tissue research · 2022Article
- Ozone-Induced Oxidative Stress, Neutrophilic Airway Inflammation, and Glucocorticoid Resistance in Asthma.Frontiers in immunology · 2021Review
- Lung macrophages: current understanding of their roles in Ozone-induced lung diseases.Critical reviews in toxicology · 2020Review
- Ozone-Induced Aryl Hydrocarbon Receptor Activation Controls Lung Inflammation via Interleukin-22 Modulation.Frontiers in immunology · 2020Article
- Nrf2 Activator RTA-408 Protects Against Ozone-Induced Acute Asthma Exacerbation by Suppressing ROS and γδT17 Cells.Inflammation · 2019Article
- Functional and morphological differences of the lung upon acute and chronic ozone exposure in mice.Scientific reports · 2018Article
- Augmented Responses to Ozone in Obese Mice Require IL-17A and Gastrin-Releasing Peptide.American journal of respiratory cell and molecular biology · 2018Article
- Neutrophilic NLRP3 inflammasome-dependent IL-1β secretion regulates the γδT17 cell response in respiratory bacterial infections.Mucosal immunology · 2017Article
- Repeated Mouse Lung Exposures to Stachybotrys chartarum Shift Immune Response from Type 1 to Type 2.American journal of respiratory cell and molecular biology · 2016Article
- Regulation of IL-17A expression in mice following subacute ozone exposure.Journal of immunotoxicology · 2016Article
- Ozone-induced IL-17A and neutrophilic airway inflammation is orchestrated by the caspase-1-IL-1 cascade.Scientific reports · 2016Article
- Deletion of mTORC1 Activity in CD4+ T Cells Is Associated with Lung Fibrosis and Increased γδ T Cells.PloS one · 2016Article
- Chronic Inflammation and γδ T Cells.Frontiers in immunology · 2016Review
- Inflammasome, IL-1 and inflammation in ozone-induced lung injury.American journal of clinical and experimental immunology · 2016Review
- All hands on DE(T)C: Epithelial-resident γδ T cells respond to tissue injury.Cellular immunology · 2015Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Ozone is an air pollutant that causes pulmonary symptoms. In mice, ozone exposure causes pulmonary injury and increases bronchoalveolar lavage macrophages and neutrophils. We have shown that IL-17A is important in the recruitment of neutrophils after subacute ozone exposure (0.3 ppm for 24-72 h). We hypothesized that γδ T cells are the main producers of IL-17A after subacute ozone. To explore this hypothesis we exposed wildtype mice and mice deficient in γδ T cells (TCRδ-/-) to ozone or room air. Ozone-induced increases in BAL macrophages and neutrophils were attenuated in TCRδ-/- mice. Ozone increased the number of γδ T cells in the lungs and increased pulmonary Il17a mRNA expression and the number of IL-17A+ CD45+ cells in the lungs and these effects were abolished in TCRδ-/- mice. Ozone-induced increases in factors downstream of IL-17A signaling, including G-CSF, IL-6, IP-10 and KC were also decreased in TCRδ-/- versus wildtype mice. Neutralization of IL-17A during ozone exposure in wildtype mice mimicked the effects of γδ T cell deficiency. TNFR2 deficiency and etanercept, a TNFα antagonist, also reduced ozone-induced increases in Il17a mRNA, IL-17A+ CD45+ cells and BAL G-CSF as well as BAL neutrophils. TNFR2 deficient mice also had decreased ozone-induced increases in Ccl20, a chemoattractant for IL-17A+ γδ T cells. Il17a mRNA and IL-17A+ γδ T cells were also lower in obese Cpefat versus lean WT mice exposed to subacute ozone, consistent with the reduced neutrophil recruitment observed in the obese mice. Taken together, our data indicate that pulmonary inflammation induced by subacute ozone requires γδ T cells and TNFα-dependent recruitment of IL-17A+ γδ T cells to the lung.
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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.