Treg细胞和PD-1/PD-L1信号通路对诱导机体免疫耐受至关重要，Treg细胞数量和功能受损，是再生障碍性贫血（AA）的重要病机；新近发现PD-1/PD-L1抑制剂的使用会导致部分肺癌患者并发AA；且我们前期研究显示，AA小鼠Treg数量减少，PD-1、PD-L1蛋白表达降低。因此，提出假说：调控PD-1/PD-L1信号的表达，促进Treg细胞发育和功能维持，直接或间接抑制效应T细胞活性，诱导免疫耐受减少造血干细胞凋亡，是改善AA免疫紊乱的新策略。本项目拟在前期基础上，以Treg细胞稳态—PD-1/PD-L1信号通路—免疫失衡所致造血干细胞凋亡为新的切入点，利用基因组学、生物信息学、分子生物学等方法，检测Treg数量与功能、PD-1/PD-L1信号通路的节点蛋白、基因及造血干细胞凋亡相关通路指标，部分揭示穿龙薯蓣皂苷诱导免疫耐受抑制造血干细胞凋亡的分子机制，为治疗AA提供实验依据。

Treg cells and PD-1/PD-L1 signaling pathway play an important role in inducing immune tolerance. The number and function of Treg cells are impaired, which is also an important pathogenesis of AA. Recent studies have found that PD-1/PD-L1 signaling pathway is a key component of maintaining immune homeostasis, and the use of its blockers can lead to AA in lung cancer patients. Previous studies found that AA model animals had significant hematopoietic disorders, the number of Treg decreased, and the expression levels of PD-1 and PD-L1 protein decreased. Therefore, Therefore, we hypothesize that regulating the expression of PD-1/PD-L1 signal, promoting the development and function of Treg cells, directly or indirectly inhibiting the activity of effector T cells, inducing immune tolerance and reducing apoptosis of hematopoietic stem cells are new strategies to improve AA immune disorder. on the basis of the previous work, this project will use modern technology methods such as genomics, bioinformatics, molecular biology, to detect the number and function of Treg cells and changes of related indicators with PD-1/PD-L1 signaling pathway and the apoptosis of hematopoietic stem cells. In order to reveal the molecular mechanism of dioscin can induce immune tolerance and inhibit apoptosis of stem cells,and provide experimental basis for the treatment of AA.