ArticleAmerican journal of physiology. Lung cellular and molecular physiology2026
Predominant lung cDC2 phenotype in cigarette smoke-exposed mice favors polarization of IL-17-producing CD4
Article in American journal of physiology. Lung cellular and molecular physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Oxidative stress-driven epigenetic reprogramming of immune cells in COPD: from epitranscriptomic and metabolic crosstalk to treatable traits.Frontiers in immunology · 2026Review
- Ferroptosis in smoke inhalation injury: from mechanisms to potential therapeutic targets.Frontiers in cell and developmental biology · 2026Review
- Interleukin-23 in lung and airway diseases: from pathogenesis to precision-guided therapeutic targeting.Frontiers in pharmacology · 2026Review
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Authors and funding
5 authors.
Funding
Abstract
Chronic obstructive pulmonary disease (COPD) is characterized by a deficiency within the lungs of regulatory T cells and an excess of Th17 cells, termed T17/Treg imbalance. Conventional dendritic cells type-1 (cDC1) and type-2 (cDC2) are known to drive Treg and Th17 polarization, respectively, but their roles in COPD are incompletely understood. Using a murine cigarette smoke (CS)-exposure model, we found that after 8 wk of CS exposure, the percentage of lung cDC1, but not cDC2, was significantly decreased (
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