Frontiers in Immunology (Nov 2017)

IL-15 Enhances Activation and IGF-1 Production of Dendritic Epidermal T Cells to Promote Wound Healing in Diabetic Mice

  • Yangping Wang,
  • Yang Bai,
  • Yashu Li,
  • Guangping Liang,
  • Yufeng Jiang,
  • Zhongyang Liu,
  • Meixi Liu,
  • Jianlei Hao,
  • Xiaorong Zhang,
  • Xiaorong Zhang,
  • Xiaohong Hu,
  • Xiaohong Hu,
  • Jian Chen,
  • Jian Chen,
  • Rupeng Wang,
  • Zhinan Yin,
  • Jun Wu,
  • Jun Wu,
  • Gaoxing Luo,
  • Gaoxing Luo,
  • Weifeng He,
  • Weifeng He

DOI
https://doi.org/10.3389/fimmu.2017.01557
Journal volume & issue
Vol. 8

Abstract

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Altered homeostasis and dysfunction of dendritic epidermal T cells (DETCs) contribute to abnormal diabetic wound healing. IL-15 plays important roles in survival and activation of T lymphocytes. Recently, reduction of epidermal IL-15 has been reported as an important mechanism for abnormal DETC homeostasis in streptozotocin -induced diabetic animals. However, the role of IL-15 in impaired diabetic wound healing remains unknown. Here, we found that, through rescuing the insufficient activation of DETCs, IL-15 increased IGF-1 production by DETCs and thereby promoted diabetic skin wound repair. Regulation of IGF-1 in DETCs by IL-15 was partly dependent on the mTOR pathway. In addition, expression of IL-15 and IGF-1 were positively correlated in wounded epidermis. Together, our data indicated that IL-15 enhanced IGF-1 production by DETCs to promoting diabetic wound repair, suggesting IL-15 as a potential therapeutic agent for managing diabetic wound healing.

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