ArticlePloS one2015
γδ T Cells Are Required for M2 Macrophage Polarization and Resolution of Ozone-Induced Pulmonary Inflammation in Mice.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 30 citations in OpenAlex.
- Prior acute ozone injury modulates inflammatory responses to subsequent repetitive ozone exposures in mice.Scientific reports · 2026Article
- Article
- Single-cell transcriptomics reveal alveolar macrophage-specific responses in single-hit ozone exposure model in mice.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Tumor-Associated Macrophages as Therapeutic Targets: Deciphering Interaction Networks and Advancing Clinical Translation.MedComm · 2026Review
- Transcriptional profiling of lung macrophages following ozone exposure in mice identifies signaling pathways regulating immunometabolic activation.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Key players of immunosuppression in epithelial malignancies: Tumor-infiltrating myeloid cells and γδ T cells.Cancer reports (Hoboken, N.J.) · 2024Review
- Immune Regulatory Networks and Therapy of γδ T Cells in Liver Cancer: Recent Trends and Advancements.Journal of clinical and translational hepatology · 2024Review
- Article
- From Host Defense to Metabolic Signatures: Unveiling the Role of γδ T Cells in Bacterial Infections.Biomolecules · 2024Review
- Vesicular and extravesicular protein analyses from the airspaces of ozone-exposed mice revealed signatures associated with mucoinflammatory lung disease.Scientific reports · 2021Article
- Compartment-specific transcriptomics of ozone-exposed murine lungs reveals sex- and cell type-associated perturbations relevant to mucoinflammatory lung diseases.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- 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
- Single-Cell Transcriptomes Reveal a Complex Cellular Landscape in the Middle Ear and Differential Capacities for Acute Response to Infection.Frontiers in genetics · 2020Article
- Ozone-Induced Aryl Hydrocarbon Receptor Activation Controls Lung Inflammation via Interleukin-22 Modulation.Frontiers in immunology · 2020Article
- Oxidative Stress in Ozone-Induced Chronic Lung Inflammation and Emphysema: A Facet of Chronic Obstructive Pulmonary Disease.Frontiers in immunology · 2020Review
- Pulmonary effects of ozone therapy at different doses combined with antibioticotherapy in experimental sepsis model.Acta cirurgica brasileira · 2020Article
- Transcriptional Profiling of the Murine Airway Response to Acute Ozone Exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Transcriptional Effects of Ozone and Impact on Airway Inflammation.Frontiers in immunology · 2019Review
- Functional and morphological differences of the lung upon acute and chronic ozone exposure in mice.Scientific reports · 2018Article
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Authors and funding
6 authors.
Funding
Abstract
We examined the role of γδ T cells in the induction of alternatively activated M2 macrophages and the resolution of inflammation after ozone exposure. Wildtype (WT) mice and mice deficient in γδ T cells (TCRδ-/- mice) were exposed to air or to ozone (0.3 ppm for up to 72h) and euthanized immediately or 1, 3, or 5 days after cessation of exposure. In WT mice, M2 macrophages accumulated in the lungs over the course of ozone exposure. Pulmonary mRNA abundance of the M2 genes, Arg1, Retnla, and Clec10a, also increased after ozone. In contrast, no evidence of M2 polarization was observed in TCRδ-/- mice. WT but not TCRδ-/- mice expressed the M2c polarizing cytokine, IL-17A, after ozone exposure and WT mice treated with an IL-17A neutralizing antibody exhibited attenuated ozone-induced M2 gene expression. In WT mice, ozone-induced increases in bronchoalveolar lavage neutrophils and macrophages resolved quickly after cessation of ozone exposure returning to air exposed levels within 3 days. However, lack of M2 macrophages in TCRδ-/- mice was associated with delayed clearance of inflammatory cells after cessation of ozone and increased accumulation of apoptotic macrophages in the lungs. Delayed restoration of normal lung architecture was also observed in TCRδ-/- mice. In summary, our data indicate that γδ T cells are required for the resolution of ozone-induced inflammation, likely because γδ T cells, through their secretion of IL-17A, contribute to changes in macrophage polarization that promote clearance of apoptotic cells.
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