创面愈合是一个极其复杂过程。树突状表皮T细胞(γδT细胞)具有促进创面愈合的重要作用，但其具体作用机制仍知之甚少。我们前期研究表明皮肤神经末梢递质Substance P具有促进γδT细胞活化作用，而最近研究提示这种活化的γδT细胞可以发挥内分泌作用，但Substance P是否调控γδT细胞参与创面愈合还有待进一步探讨。为此，我们提出假说，在皮肤创面损伤刺激下诱发神经末梢释放Substance P，进而激活γδT细胞发挥内分泌作用，通过神经-免疫-内分泌轴调控角质细胞促进创面愈合。为了验证这一假说，我们将利用基因敲除小鼠等工具，细胞、组织(共)培养等方法和技术，从体内、体外两个角度，分别在分子、细胞、整体等不同水平探讨Substance P调控γδT细胞促进创面愈合的作用和机制。本研究将从神经-免疫-内分泌轴这一新视点为揭示创面愈合的发生机制奠定基础，为临床创面愈合防治提供新的思路。

Accumulating evidence show that dendritic epidermal T cell (γδT cell, DETC) plays an essential role in the wound healing process, but the underlying mechanisms behind it remain unclear. Based on our previous findings that Substance P activates γδT cells, and recently, γδT cells have also been demonstrated that they exert endocrine effects. However, how substance P modulate γδT cell to promote wound healing needs further investigation. Thus, we hypothesis that substance P activate γδT cell to exert endocrine effects, thereby to promote wound healing. To clarify this issue, here, by knockout mice, skin organ culture model, etc, we aim to investigate that the potential role and the underlying mechanisms of Substance P on the production of NGF by γδT cells to promote wound healing. These findings will uncover a novel mechanism of neuro-immuno-endocrine modulation in the wound healing and provide a potential therapy for the treatment of wound.