肝脏缺血再灌注损伤常发生于各类肝脏手术，严重影响患者的术后康复。近年来，借助调控免疫负性调节细胞干预受损肝脏的炎症进展已成为新治疗思路之一。前期研究证实，髓源性抑制细胞（Myeloid-Derived Suppressor Cell, MDSC）在缺血再灌注损伤肝脏中浸润增多，且同步升高表达的趋化因子C-C基序配体15（C-C motif chemokine ligand 15, CCL15）、Yes相关蛋白（yes associated protein, YAP）可能是关键调控因子。因此，本课题将系统探究肝细胞通过YAP-CCL15通路趋化MDSC抗缺血再灌注损伤的作用机制，主要阐明：（1）肝细胞在缺血再灌注损伤后通过激活YAP，调控CCL15基因的表达；（2）受损肝脏分泌的CCL15结合外周MDSC表面受体，诱导其募集；（3）在肝损病灶周围，浸润的MDSC发挥抗炎作用。

Liver ischemia-reperfusion injury often occurs during liver surgery, which seriously impedes the postoperative recovery and long-term quality of life of patients. Recently, managing the inflammatory progression in the injured liver by regulating negative immune-regulating cells has become a new therapeutic idea. Our previous study confirmed that the infiltration of myeloid-derived suppressor cell (MDSC) enhanced in the liver ischemia-reperfusion injury course. Besides, chemokine C-C motif chemokine ligand 15 (CCL15) and yes associated protein (YAP), which increased coordinately after liver injury, might be the key regulator. In this subject, the mechanism that hepatocytes recruit MDSC cells against ischemia-reperfusion injury through YAP-CCL15 pathway will be systematically investigated, including: (1) after ischemia-reperfusion injury, hepatocytes promote the transcriptional activation process of CCL15 gene by activating the YAP pathway; (2) CCL15 secreted from the damaged liver can bind to the surface receptor of peripheral MDSC, which recruits MDSC into intrahepatic lesions; (3) the infiltrated MDSC can inhibit the inflammatory response in the liver lesion.