Frontiers in Immunology (Feb 2018)

Vγ4 T Cells Inhibit the Pro-healing Functions of Dendritic Epidermal T Cells to Delay Skin Wound Closure Through IL-17A

  • Yashu Li,
  • Yangping Wang,
  • Lina Zhou,
  • Meixi Liu,
  • Meixi Liu,
  • Guangping Liang,
  • Rongshuai Yan,
  • Yufeng Jiang,
  • Jianlei Hao,
  • Xiaorong Zhang,
  • Xiaorong Zhang,
  • Xiaohong Hu,
  • Xiaohong Hu,
  • Yong Huang,
  • Yong Huang,
  • Rupeng Wang,
  • Zhinan Yin,
  • Jun Wu,
  • Jun Wu,
  • Jun Wu,
  • Gaoxing Luo,
  • Gaoxing Luo,
  • Weifeng He,
  • Weifeng He

DOI
https://doi.org/10.3389/fimmu.2018.00240
Journal volume & issue
Vol. 9

Abstract

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Dendritic epidermal T cells (DETCs) and dermal Vγ4 T cells engage in wound re-epithelialization and skin inflammation. However, it remains unknown whether a functional link between Vγ4 T cell pro-inflammation and DETC pro-healing exists to affect the outcome of skin wound closure. Here, we revealed that Vγ4 T cell-derived IL-17A inhibited IGF-1 production by DETCs to delay skin wound healing. Epidermal IL-1β and IL-23 were required for Vγ4 T cells to suppress IGF-1 production by DETCs after skin injury. Moreover, we clarified that IL-1β rather than IL-23 played a more important role in inhibiting IGF-1 production by DETCs in an NF-κB-dependent manner. Together, these findings suggested a mechanistic link between Vγ4 T cell-derived IL-17A, epidermal IL-1β/IL-23, DETC-derived IGF-1, and wound-healing responses in the skin.

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