Changes and clinical significance of CD8(+) T cell subset in patients with aplastic anemia, myelodysplastic syndrome and acute myeloid leukemia

Abstract

This study was purposed to detect the balance and the activity change of cytotoxic T cell subsets in aplastic anemia (AA) patients, myelodysplastic syndrome (MDS) patients and acute myeloid leukemia (AML) patients, and to explore the cellular immune mechanism for abnormal hematopoiesis of the three diseases, so as to provide experimental basis for the choice of clinical treatment. The proportion of the cytotoxic T cells and part of the T-cells subsets in peripheral blood were detected by flow cytometry in 35 cases of MDS, including 19 refractory anemia (MDS-RA), 16 refractory anemia with excess blasts (MDS-RAEB), 17 AA, 15 AML patients and 10 normal donors respectively. The results showed that compared with the control group, the percentage of Tc1, Tc1/Tc2, CD8(+)HLA-DR(+), CD3(+)CD8(+)CD28(+), CD8(+)CD45RO(+) cells was significantly higher and the percentage of CD8(+)CD45RA(+) was significantly lower in AA and MDS-RA group. There was no difference in the percentage of Tc2 cells between AA/MDS-RA and normal controls; the percentage of CD8(+)CD45RO(+) cells was significantly higher and the percentage of Tc1, CD3(+)CD8(+)CD28(+), CD8(+)HLA-DR(+) was significantly lower in MDS-RAEB group, the percentage of CD8(+)CD45RA(+) was lower but the difference was not significant, and there was no difference in the percentage of Tc, Tc1/Tc2 cells between MDS-RAEB group and the control group. The percentage of Tc2 cells was significantly higher and the percentage of other parameters was significantly lower in AML group than those of normal controls. It is concluded that the cellular immune statuses in AA, the different stages of MDS and AML are different. In AA and the early stage of MDS, the balance of Tc1/Tc2 shifts to Tc1, and the activation of T-cell subsets increases. In the late stage of MDS and AML, the balance of Tc1/Tc2 shifts to Tc2, the activation of T-cell subsets decreases. The former may be closely related to bone marrow failure while the latter may be one of the important mechanisms in which the malignant clones escape from immune effect.