红细胞Rh血型系统的D抗原具有重要的临床意义，其编码基因是RHD。输血供受者或胎母间的D抗原表型不同，可能引起严重的输血反应或新生儿溶血病。申请者前期在对D抗原遗传机制的研究中，发现部分个体的RHD基因分型和预期的D抗原表达不一致。根据其他报道和我们的前期实验结果，我们推测：D抗原在伴随红系分化的表达过程中，可能在转录水平受KLF7转录因子的调控；而miR-146b可能通过靶向调控KLF7，进而引起其下游调控目的蛋白RhD和携带的D抗原表达异常。我们将通过EMSA、CHIP、双荧光素酶报告基因检测、过表达和抑制表达慢病毒感染、WB、qRT-PCR、流式检测等方法，验证红系分化过程中KLF7对RHD基因的表达调控作用，以及该过程中KLF7是否受miR-146b的靶向调控。本项研究的结果有助于了解红系分化过程中血型抗原的表达机制，并有助于D抗原的正确分型和配合型输注。

The D antigen of the Rh blood group system on red blood cells has important clinical significance, which is encoded by RHD gene. The discrepancies of D antigen phenotypes between blood transfusion recipients and blood donors or between mothers and fetuses possibly lead to severe transfusion reaction and hemolytic diseases of the fetus and newborn. In the previous studies of the genetic mechanisms of the D antigen conducted by the applicant, inconsistent D antigen expressions and RHD genotyping results were found in some individuals. According to other published reports and our previous results, we hypothesize that the expression of D antigen is probably regulated by KLF7 transcription factor at transcription level during erythroid differentiation. Moreover, miR-146b might lead to abnormal expression of KLF7's downstream target RhD and the D antigen carried by RhD protein through targeting KLF7. We will validate the target regulation of miR-146b on KLF7 and further roles in the regulation of D antigen expression during erythroid differentiation, by the methods of EMSA, CHIP, dual-luciferase reporter assays, overexpression and suppression lentivirus infections, WB, qRT-PCR, as well as flow cytometry, and so on. The results of this research will contribute to the understanding of the regulative mechanism of blood group antigens during erythroid differentiation, and help correct typing of D antigen and the compatible transfusion.