Thl7是新发现的一类CD4+T细胞亚群，在移植排斥包括慢性排斥中的作用已受到广泛关注。我们在临床研究中发现肝移植术后血清IL-17升高常伴随排斥反应发生，此时患者外周血RANKL+淋巴细胞的比例明显增加，这部分细胞分泌IL-17能力较强，提示RANKL信号与Thl7分化及功能有一定关系,体外预实验证实RANKL信号参与调控Th17分化及功能，但具体机制如何？体内是否有相似作用以及是否可以作为肝移植排斥干预靶点？尚不清楚。基于此，本课题拟研究RANKL信号对Th17分化、表型和功能的影响及机制；抗原提呈过程RANKL信号对Th17免疫学功能的影响及机制；Rag-2-/-小鼠为受者观察活化或抑制RANKL信号的Th17回输后，allo-DTH的变化；建立小鼠肝脏移植模型观察RANKL信号对Th17参与排斥反应的影响及机制，为进一步认识肝移植排斥发生机制并探寻干预策略提供新的途径及实验数据。

Th17 is a newly discovered subgroup of CD4+ T cell and its role in transplant rejection has received extensive attention. Clinical studies showed that increased serum IL-17 after liver transplantation is often accompanied with the occurrence of chronic rejection, and the proportion of RANKL+ lymphocytes, which secrete plenty of IL-17, in peripheral blood increased significantly. It implicated that RANKL signal is relevant with differentiation and function of Th17. In vitro preliminary study confirmed that RANKL signal involved in the regulation of Th17 differentiation and function. But the exact mechanism and whether it can be utilized in the treatment of liver transplant rejection are still unknown. Based on this, the subject is to study the effect of RANKL signals on the regulation of Th17 differentiation, phenotype and function; to elucidate the effect of RANKL signal on Th17 immunological function during antigen presenting; to observe the effect of reinfusing Th17 which activate or inactivate RANKL signal on all-DTH by setting Rag-2-/-mice as recipients; to research the effect and mechanism of RANKL signal on Th17-involved rejection, for a better understanding of the effect of Th17 differentiation and functional regulation in transplant rejection.