Some patients with CML can withdraw from TKIs after treatment, and the mechanism might be related to the effect of memory NK cells on anti-Ph+ leukemic stem cells (LSCs). Dasatinib affects immune through several pathways including the expression of PD1 in immune cells. Our previous work showed increased NKG2C+ NK cells were found in cases with CMV-DNA+ who suffered Ph+ leukemia and received Dasatinib, and these memory NK cells have anti-LSCs activity. We hypothesize that: CMV infection activates NKG2C+ memory NK cells proliferation; Dasatinib down-regulates the expression of PD1 in PD1+NKG2C+ NK cell subsets and then enhances anti-LSCs activity of these cells. In this study, the effect of Dasatinib on CMV-activated NKG2C+ cell subsets and its mechanism will be studies. Besides, the different NKG2C+ cell subsets on LSCs will be compared. This study might be helpful to clarify the mechanism of TKI withdrawal and to offer foundation for CMV and Ph+ ALL treatment strategies
Research on the mechanism of dasatinib down-regulates the expression of PD-1 in CMV-activated NKG2C+NK cells and enhances killing pH + leukemia stem cells.