ArticleNature communications2025
Comprehensive profiling of smoke-induced T cells in mice implicates clonal γδT17 cells as a hallmark of COPD.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Dual role of IL-17A in COPD: amplifier of inflammatory cascades and mediator of airway remodeling and alveolar destruction.Frontiers in immunology · 2026Review
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Authors and funding
27 authors.
Funding
Abstract
The mechanisms of the chronic inflammatory response in smoking-induced chronic obstructive pulmonary disease (COPD) remain unclear, with limited understanding of T cell responses to smoke exposure in lung tissue and circulation. We characterized the alterations in T cells associated with smoke exposure using single-cell RNA sequencing, TCR sequencing, and flow cytometry-based validation. Our experiments show significant recruitment of T cells within the airways, exhibiting a multifaceted immune profile, augmented TCR clonal diversity, and a prolonged CDR3 length. Notably, smoke-induced γδ T cells, particularly clonally expanded γ6δ4 T cells with high Il17a expression, accumulate in smoke-induced airway inflammation. Despite arising in inflammation, these cells function in a protective manner: γδT17 deficiency worsens smoke-induced lung injury, whereas adoptive transfer of γδT17 cells restores tissue protection in smoke-exposed lungs over time. Here, we show γδT17 cells as a potential target for addressing smoke-induced immune dysfunctions, providing alternative avenues for early prevention and treatment of COPD.
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