急性细胞性排斥反应（ACR）是导致器官移植失败的严重并发症之一。树突状细胞（DC）除了在二级淋巴器官中进行抗原提呈功能外，其在移植物中参与介导ACR的相关机制尚不明确。申请人前期研究表明宿主单核细胞分化来的DC(Mono-DC)在ACR的发生中发挥着重要作用，且这些宿主Mono-DC高表达趋化因子受体CX3CR1。此外，CX3CR1通路在炎症组织中不仅可以促使单核细胞迁移，还能刺激淋巴细胞活化。因此，我们推测宿主Mono-DC在移植物中介导ACR的发生与CX3CR1通路十分相关。本研究以CX3CR1基因敲除小鼠的心脏与肾脏移植模型为研究对象，通过结抗剂干预、流式细胞和双光子荧光显微镜技术探讨：（1）CX3CR1通路在宿主Mono-DC迁入移植物中的作用及机制，（2）CX3CR1通路对宿主Mono-DC刺激效应T细胞从而介导ACR的影响及机制，以期为器官移植后ACR的防治提供新思路。

Acute cellular rejection (ACR) is one of the most severe complications, which cause transplant organ failure. In addition to antigen presentation in secondary lymphatic organs, the related mechanism of dendritic cell (DC) mediating ACR in graft is still not clear. Based on our previous study, the host monocyte-derived DC (Mono-DC) play a crucial role in ACR after transplantation, and these host Mono-DC highly express chemokine receptor CX3CR1. Besides, CX3CR1 pathway not only helps monocyte migration but stimulates and activates lymphocytes in inflammatory tissue. Hence, we deduce CX3CR1 pathway could be associated with host Mono-DC mediating ACR in graft. Using antagonist interference, flow cytometry and two-photon intravital microscopy, we intend to investigate several issues via setting up CX3CR1 knockout mice heart and kidney transplanted models as follows: (1) the role of CX3CR1 pathway in host Mono-DC migration to graft; (2) the mechanism of host Mono-DC stimulating T effector cell to cause ACR via CX3CR1 pathway. Our study may provide novel theory into the pathogenesis, prophylaxis and treatment of ACR to instruct clinical practice.