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<p>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 <i>Il17a</i> 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.</p>

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

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年12月8日

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

摘要

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.