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<p>Lung ischemia-reperfusion injury (LIRI) is a serious complication in critical clinical situations. Despite its importance, the specific role of type II natural killer T (NKT) cells in LIRI remains unclear. In this study, we establish a LIRI mouse model and demonstrate that sulfatide-reactive type II NKT cells promote M2 polarization of alveolar macrophages (AMs) and alleviate LIRI through AMs-mediated mechanisms. This protective effect is absent in <i>Jα18</i><sup><i>−/-</i></sup> mice, indicating the essential role of invariant NKT (iNKT) cells. Further analysis shows that interleukin-10 (IL-10) secreted by iNKT cells upregulates AT-rich interaction domain 3 A (Arid3a) in macrophages, which then promotes the transcription of DNA damage inducible transcript 4 (DDIT4). This cascade enhances M2 polarization of macrophages, potentially contributing to lung protection and alleviating LIRI. These findings suggest that NKT cells may offer a therapeutic target for LIRI in the future.</p><p></p>

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Functional remodeling of iNKT cells by sulfatide-reactive type II NKT cells reprograms alveolar macrophages to alleviate lung ischemia-reperfusion injury

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月17日

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  • Qingqing Li,
  • Jing Yin,
  • Qibin Lin,
  • Yaqing Xu,
  • Jilong He,
  • Xiu Shi,
  • Sisi Huang,
  • Yunfan Wang,
  • Yi Huang,
  • Xuhong Ding,
  • Hongying Yu,
  • Hanxiang Nie

摘要

Lung ischemia-reperfusion injury (LIRI) is a serious complication in critical clinical situations. Despite its importance, the specific role of type II natural killer T (NKT) cells in LIRI remains unclear. In this study, we establish a LIRI mouse model and demonstrate that sulfatide-reactive type II NKT cells promote M2 polarization of alveolar macrophages (AMs) and alleviate LIRI through AMs-mediated mechanisms. This protective effect is absent in Jα18−/- mice, indicating the essential role of invariant NKT (iNKT) cells. Further analysis shows that interleukin-10 (IL-10) secreted by iNKT cells upregulates AT-rich interaction domain 3 A (Arid3a) in macrophages, which then promotes the transcription of DNA damage inducible transcript 4 (DDIT4). This cascade enhances M2 polarization of macrophages, potentially contributing to lung protection and alleviating LIRI. These findings suggest that NKT cells may offer a therapeutic target for LIRI in the future.