克服白血病患者T细胞免疫功能缺陷而改善预后仍是关键问题。我们前期发现尽管急性髓性白血病(AML)病人存在白血病相关的γδ T细胞克隆，但免疫激活性受体NKG2D表达水平下降，而高表达免疫抑制性受体PD-1的γδ T细胞亚群影响患者预后。故推测这些免疫抑制性受体可能是介导AML中γδ T细胞免疫功能抑制及耗竭的重要原因之一。因此本课题拟综合分析AML患者体内γδ T细胞功能亚群相关免疫抑制性受体（CTLA-4，Tim-3，TIGIT，LAG-3和BTLA等）改变情况及其与γδ T细胞功能耗竭程度的关系，鉴定与预后相关的耗竭性γδ T细胞表型特征，分析调控耗竭性γδ T细胞中NKG2D的表达后，γδ T细胞表型和活化功能包括抗AML效应等逆转的可能性，通过转录组测序分析逆转效应的相关通路分子机制，为AML病人的γδ T细胞免疫治疗提供新策略。

How to reivse the T cell immunodeficiency to improve prognosis of leukemia is worthy to further investigate. Our previous study identified clonally expanded γδ T cell clone in blood from acute myeloid leukemia (AML) patients, however, the expression level of immune activated receptor NKG2D decreased, moreover some of γδ T cell subfamilies with high immune inhibited receptor PD-1 were related to poor prognosis Therefore, we hypothesize that the immune inhibited receptors may play an important role in the functional deficiency and exhaustion of γδ T cell immune response in AML patients. In this study, we intend to analyze the relationship between the alternations of the immune inhibited receptors (CTLA-4, Tim-3, TIGIT, BTLA, et la.) that related to the different γδ T cell subfamilies and the degree of γδ T cell functional exhaustion, and characterize the exhausted γδ T cell which related to the prognosis. On the other hand, through regulating the expression of NKG2D in exhausted γδ T cell, we will analyze the phenotype and activation function of γδ T cell, including the possibility of functional reversion with anti-leukemia effects. Most importantly, we will investigate the molecular mechanism of the reversion effect by using the RNA-seq,. Together, the study is expected to provide a new immunotherapy strategy for AML patients.