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Background <p>Group 2 innate lymphoid cells (ILC2s) are recognized as key innate immune effectors that facilitate early cardiac recovery after myocardial infarction (MI); however, the underlying mechanisms by which they mediate this repair remain largely unclear.</p> Methods <p>To investigate the role of ILC2-derived interleukin-9 (IL-9), we employed ILC2-specific IL-9 knockout mice and administered exogenous IL-9 in a murine MI model. The mechanism of regulatory T cells (Tregs) activation was further examined through Treg-specific Sirt1 knockout in vitro, focusing on STAT5 acetylation and related signaling.</p> Results <p>We demonstrate that ILC2-derived IL-9 is essential for post-MI repair by activating Tregs. IL-9 binding to the IL-9 receptor on Tregs upregulates the deacetylase Sirt1, and Sirt1 deletion abolishes IL-9-driven Treg activation. Furthermore, Sirt1 directly interacts with STAT5, promoting its deacetylation and phosphorylation, leading to the transcriptional activation of genes essential for Treg function.</p> Conclusion <p>Our study identifies IL-9 as a key regulator of Treg activation via a novel Sirt1-STAT5 epigenetic pathway, which promotes tissue repair after MI. These findings reveal a previously unrecognized immunomodulatory axis with significant therapeutic potential for ischemic heart disease.</p>

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ILC2-derived IL-9 activates regulatory T cells to facilitate post-myocardial infarction repair

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月27日

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  • Yuxiao Feng,
  • Rongjiao Shao,
  • Yiping Shi,
  • Haibei Sun,
  • Chen Chi,
  • Weizhuo Liu,
  • Bin He,
  • Wenzheng Han,
  • Xumin Hou

摘要

Background

Group 2 innate lymphoid cells (ILC2s) are recognized as key innate immune effectors that facilitate early cardiac recovery after myocardial infarction (MI); however, the underlying mechanisms by which they mediate this repair remain largely unclear.

Methods

To investigate the role of ILC2-derived interleukin-9 (IL-9), we employed ILC2-specific IL-9 knockout mice and administered exogenous IL-9 in a murine MI model. The mechanism of regulatory T cells (Tregs) activation was further examined through Treg-specific Sirt1 knockout in vitro, focusing on STAT5 acetylation and related signaling.

Results

We demonstrate that ILC2-derived IL-9 is essential for post-MI repair by activating Tregs. IL-9 binding to the IL-9 receptor on Tregs upregulates the deacetylase Sirt1, and Sirt1 deletion abolishes IL-9-driven Treg activation. Furthermore, Sirt1 directly interacts with STAT5, promoting its deacetylation and phosphorylation, leading to the transcriptional activation of genes essential for Treg function.

Conclusion

Our study identifies IL-9 as a key regulator of Treg activation via a novel Sirt1-STAT5 epigenetic pathway, which promotes tissue repair after MI. These findings reveal a previously unrecognized immunomodulatory axis with significant therapeutic potential for ischemic heart disease.