Comprehensive profiling of smoke-induced T cells in mice implicates clonal γδT17 cells as a hallmark of COPD

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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Publication Details

Journal
Nature Communications
Published
2025-12-08
DOI
https://doi.org/10.1038/s41467-025-67120-w
Primary Topic
Chronic Obstructive Pulmonary Disease (COPD) Research
Type
article
Field-Weighted Citation Impact
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article

Comprehensive profiling of smoke-induced T cells in mice implicates clonal γδT17 cells as a hallmark of COPD

Yumin Zhou, Suyin Huang, Ge Bai, Mingzhu Huang et al.
Nature Communications
Chronic Obstructive Pulmonary Disease (COPD) Research
article

Comprehensive profiling of smoke-induced T cells in mice implicates clonal γδT17 cells as a hallmark of COPD

Yumin Zhou, Suyin Huang, Ge Bai, Mingzhu Huang, Qi Wen, Peiyu Huang, Zhongfang Wang, Xiaoyang Zheng, Jieda Cui, Xinyue Mei, Junxiang Wang, Pixin Ran, Erkang Yi, Fan Wu, Cheng Li, Xiaoyu Wang, Jingwei Zhang, Yü Liu, Xinyuan Liu, Qi Wan, Xiaohui Wu, Yuan Wang, Ruiting Sun, Jiaying Zhong, Ziqing Yuan, Leqing Zhu, Yujie Zuo
article en

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.

Nature CommunicationsVol. 17(1)
Guangzhou Experimental Station (CN), First Affiliated Hospital of Guangzhou Medical University (CN), Nanfang Hospital (CN), State Key Laboratory of Respiratory Disease (CN), Hainan Medical University (CN), Guangzhou Medical University (CN)
Openalex Percentile: Top 43%
Chronic Obstructive Pulmonary Disease (COPD) Research
DOIOpen Access PDFOpenAlex
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