Objective: To investigate the association between the T cell inhibitory receptor programmed death 1(PD-1)and T cell exhaustion status in T cells from patients with de novo acute myeloid leukemia(AML) and AML in complete remission(CR).Methods:Surface expression of PD-1 and the exhaustion and immunosenescence markers CD244 and CD57 on CD3+,CD4+ and CD8+ T cells from peripheral blood samples from 20 newly diagnosed,untreated AML patients and 10 cases with AML in CR was analyzed by flow cytometry.Twenty-three healthy individuals served as control.Results:A significantly higher percentage of PD-1+ cells were found for CD3+ T cells in the de novo AML group compared with healthy controls.In addition,an increased level of PD-1+ CD8+ T cells,but not PD-1+ CD4+,was found for CD3+ T cells in the de novo AML and AML-CR samples.A higher percentage of CD244+ CD4+,CD244+ CD8+,CD57+ CD4+ and CD57+ CD8+ T cells was found in CD3+ T cells in samples from those with de novo AML compared with those from healthy controls.Strong increased PD-1+ CD244+ and PD-1+ CD57+ coexpression was found for CD4+ and CD8+ T cells in the de novo AML group compared with healthy controls.Conclusions:We characterized the major T cell defects,including co-expression of PD-1 and CD244,CD57-exhausted T cells in patients with de novo AML,and found a particular influence on CD8+ T cells,suggesting a poor anti-leukemia immune response in these patients. Objective: To investigate the association between the T cell inhibitory receptor programmed death 1 (PD-1) and T cell exhaustion status in T cells from patients with de novo acute myeloid leukemia (AML) and AML in complete remission (CR). Methods: Surface expression of PD-1 and the exhaustion and immunosenescence markers CD244 and CD57 on CD3 +, CD4 + and CD8 + T cells from peripheral blood samples from 20 newly diagnosed, untreated AML patients and 10 cases with AML in CR was analyzed by flow cytometry. Twenty- Three healthy individuals served as control. Results: A significant higher percentage of PD-1 + cells were found for CD3 + T cells in the de novo AML group compared with healthy controls. In addition, an increased level of PD-1 + CD8 + T cells , but not PD-1 + CD4 +, was found for CD3 + T cells in the de novo AML and AML-CR samples. A higher percentage of CD244 + CD4 +, CD244 + CD8 +, CD57 + CD4 + and CD57 + CD8 + T cells was found in CD3 + T cells in samples from those with de novo AML compared with those from he althy controls.Strong increased PD-1 + CD244 + and PD-1 + CD57 + coexpression was found for CD4 + and CD8 + T cells in the de novo AML group compared with healthy controls. Conclusions: We characterized the major T cell defects, including co-expression of PD-1 and CD244, CD57-exhausted T cells in patients with de novo AML, and found a particular influence on CD8 + T cells, suggesting a poor anti-leukemia immune response in these patients.