调节性T细胞(Tregs)可通过免疫抑制作用阻止免疫系统对造血干/祖细胞(HSPCs)的杀伤，从而促进HSPCs的存活及自我更新。但迄今对Tregs直接促进白血病细胞干性的作用和机制所知甚少。而且白血病干细胞(LSCs)是白血病复发和化疗耐药的根源。因此，研究Tregs对白血病细胞干性的调控作用可了解白血病复发的关键机制。在我们前期研究中，检测了急性髓系白血病患者骨髓中Tregs与LSCs的比例，发现两者呈正相关，而且Tregs可增加白血病细胞侧群细胞比例及集落形成能力。在此基础上，本项目以Tregs促进白血病细胞干性为假设，将通过Tregs与白血病细胞共培养体外明确Tregs对白血病细胞干性的影响，使用AML1-ETO小鼠发病模型及PDX模型体内验证Tregs对起始白血病的影响，并将深入探索Tregs对白血病细胞干性的调控机制。旨在为靶向LSCs的治疗提供科学依据。

Regulatory T cells (Tregs) can protect normal hematopoietic stem/ progenitor cells (HSPCs) from immune destruction through immunosuppression, and promote the survival and self-renew of HSPCs. But little was known about the role and mechanism that Tregs might directly promote the stemness of leukemia cells. It has been reported that leukemia stem cells (LSCs) are the basis of leukemia relapse and chemoresistance. So, investigating Tregs regulating the stemness of leukemia cells will help us to know the mechanism of leukemia relapse. Our recent results showed a positive correlation between the proportions of Tregs and LSCs in the bone marrow of acute myeloid leukemia patients; Tregs can increase the proportion of side population cells and promote the ability of colony formation in vitro. In this study, we propose the hypothesis that Tregs can promote the stemness of leukemia cells, and validate it by following experiments: 1) to make sure that Tregs increase the population of LSCs in vitro; 2) to find the related signal pathway on stemness regulation of leukemia cells ; 3) to verify the function and related mechanism of Tregs in promoting the stemness of leukemia cells in animal models. From this study, we want to provide a scientific basis for new treatment strategies of targeting leukemia stem cells.