OBJECTIVE: To investigate the inhibitory effects of dasatinib on proliferation, 
function, and signaling events on CD8+T cells.
MATERIALS AND METHODS: Carboxyfluorescein diacetate succinimidyl ester and 
5-bromo-2-deoxyuridine were used to detect proliferation and cell cycle of CD8+T 
cells treated with dasatinib, respectively. Frequency and function of viral and 
leukemia-antigen-specific CD8+T cells from healthy donors were measured by 
tetramer staining and ELISPOT assay. Western blotting analysis was performed to 
detect T-cell receptor (TCR), nuclear factor kappa B (NF-kappaB) and Src 
signaling events in T cells treated with dasatinib or imatinib.
RESULTS: Dasatinib inhibited proliferation of CD8+T cells in a dose-dependent 
manner, which was associated with lower secretion of interferon-gamma and 
granzyme B, as well as with arrest of CD8+T cells in the G0/G1 phase of cell 
cycle. Inhibition of CD8+T cells was proven for blood samples from a patient 
under dasatinib medication when compared with their T-cell status without 
dasatinib. Western blotting confirmed that these effects were mediated through 
downregulation of the phosphorylation level of molecules from the TCR and the 
NF-kappaB signaling transduction cascade. Dasatinib proved to be more potent 
than imatinib on Src and TCR signaling events in Jurkat T cells.
CONCLUSION: Our study demonstrated that dasatinib impaired proliferation and 
function of CD8+T cells via TCR and NF-kappaB signaling events without inducing 
apoptosis. Therefore, dasatinib might alter the graft-vs-leukemia effect and the 
graft-vs-host disease after allogeneic stem cell transplantation sustained by 
CD8+T cells. Dasatinib might also be used as a novel immunosuppressant agent.