急性移植物抗宿主病（aGVHD）是异基因造血干细胞移植最致命的并发症，病因复杂。我们的研究发现，microRNA155（miR155）在aGVHD发生时显著升高，与Th17数量及血浆IL-17a表达呈正相关。感染编码信号转导和转录激活因子3（STAT3）在miR155基因启动子部位异常丰富，与aGVHD靶器官中Th17聚集密切相关。由此推测：miR155/STAT3途径可通过调控Th17参与aGVHD。本项目拟①扩大aGVHD临床数据明确miR155/STAT3与Th17的相互关系；②体外实验探讨miR155对Th17的调控是否依赖STAT3途径；③以miR155基因缺陷和CD4-STAT3 KO鼠的aGVHD模型，体内验证miR155/STAT3对aGVHD的作用机制。本研究旨在明确miR155/STAT3调控的Th17在aGVHD中的作用，以阐明疾病的发病机理，为靶向治疗提供理论依据。

Acute graft-versus-host disease(aGVHD) is the most serious complication of hematopoietic stem cell transplant, the mechanism is complex. Research declared that Th17 cell aggravated aGVHD, our previous study showed that miR-155 expression is up-regulated in the serum from patients with aGVHD. Serum IL-17 level and the proportions of Th17 cell are positively correlated with miR-155 level in aGVHD patients. New research showed that STAT3 signaling and resultant Th17 tissue accumulation is closely associated with acute GVHD. STAT3 ChIP-qPCR showed that enrichment of STAT3 around the promoter region of miR-155. We speculated Th17 cell may participate in aGVHD pathophysiology by miR-155/STAT3 signal. In this project, we analyze miR-155、STAT3 among Th17 cell from more allogeneic HCT recipients. In vitro experiments, we analyze the expression profile of miR-155 among T cell, and further a functional link between STAT3 and miR-155 in the regulation of Th17 differentiation. We use genetic defect miR155 mouse model 、CD4-STAT3 KO mouse model and haploid transplantation mouse model as the experimental platform, explore the molecular mechanism of STAT3 regulating miR155 expression in Th17 cells in aGVHD. This study will help understand the role of miR155/STAT3 regulation in Th17 cells in aGVHD situation, in order to elucidate the pathogenesis of aGVHD, provide theoretical basis for clinical treatment of aGVHD.