复发是AML患者allo-HSCT后死亡的首要原因，而白血病细胞逃逸免疫监视是其中关键环节。目前认为NK细胞在白血病复发监视中发挥重要作用，而包括AML在内多种肿瘤细胞能通过降低或缺失NKG2D配体ULBP的表达从而逃脱NK细胞杀伤，但具体机制尚不明确。我们前期研究发现C/EBPα编码基因CEBPA突变在AML移植后复发中发挥作用，进一步研究显示在AML细胞株中过表达C/EBPα能明显增加ULBP表达，并增强白血病细胞对NK杀伤敏感性，而CEBPA突变则降低白血病细胞对NK杀伤敏感性。因此我们认为C/EBPα能通过调节ULBP表达从而调控NKG2D介导的免疫杀伤作用，但具体机制及其在白血病复发中的作用尚不明确。本课题拟从体外、体内和动物水平研究C/EBPα及其突变体对ULBP的调节作用及其分子机制，明确CEBPA突变在白血病逃逸NKG2D介导的杀伤中的作用，为AML复发的治疗提供理论基础。

Relapse is the first reason of death in AML patients received allo-HSCT. AML cells evading of immune surveillance is the key process of AML relapse. The recent studies have shown that NK cells play an important role in the surveillance of AML relapse. However, many tumor cells including AML cells decline their NKG2D ligands expression to escape from being killed by NK cells. The mechanisms involved have not been revealed yet. Our previous study showed that multiple CEBPA mutations contribute to leukemia relapse after allo-HSCT. Further we found that over-expressing C/EBPα in AML cell lines significantly up-regulated the expression of ULBPs and enhanced their sensibility to the killing effect of NK cells. But the expression of ULBPs and cells’ sensibility to NK cells was decreased when C/EBPα coding gene CEBPA was mutant. Based on these results, we consider that C/EBPα regulates the anti-tumor immunity induced by NKG2D receptor through regulating the expression of ULBPs. Our reaserch intends to demonstrate the regulatory effect of C/EBPα in vitro and in vivo on the anti-tumor immunity induced by NKG2D receptor, which will provide theoretical basis for the treatment of AML relapse.