心脏移植物血管病变导致心脏移植物慢性失功，是目前移植领域研究的难点和热点。我们的动物和临床实验均表明NKG2D/Ligand 与心脏移植物血管病变密切相关，但具体机制不明。据此，本项目拟利用条件性基因敲除鼠，观察阻断NKG2D/Ligand减轻心脏移植物血管病变的作用及机制，检测心脏移植物内γδ T、NK、 DC细胞的表达水平、Mφ及其功能亚群（AAM/CAM）、T细胞功能亚群（Th17/Treg、Th1/Th2、Th9、Th22等）的分化和功能、体液免疫(MICA、C4d、AECA、CM、AT1R、Col V等)的水平、心脏冠状血管组织细胞及心肌细胞的激活、增殖和功能状态。同时深入探讨γδ T细胞在心脏移植物血管病变中的作用，为临床有效治疗心脏移植物血管病变提供新的靶点。

Cardiac allograft vasculopathy (CAV) leading to chronic allgoraft dysfunction has been the difficulty and hot spot in the area of transplantation. Our experimental and clinical studies have demonstrated that NKG2D/Ligand was closely related to CAV and the mechanism was still unclear. Hereby, this project will observe effect and mechanism of NKG2D/Ligand blockade alleviating CAV, based on conditional knockout mice, and detect the expression levels of γδ T, NK and DC cells, the differentiation and function of macrophage subgroups (AAM/CAM) and T cell subgroups (Th17/Treg, Th1/Th2, Th9, Th22), the levels of humoral rejection response (MICA, C4d, AECA, CM, AT1R,Col V), the activation, proliferation and function of cardiac coronary tissue cells and myocardial cells. We will furtherly investigate the function of γδ T cells in CAV. This will provide new target for treatment of CAV.