[Expression of miR-16 in patients with T lymphoblastic lymphoma/acute lymphoblastic leukemia].

This study was purposed to investigate the expression of miR-16 in T lymphoblastic lymphoma/acute lymphoblastic leukemia (T-LBL/ALL) and its relation with target therapy and prognosis. The CD3, cCD3, CD10, CD20, CD34, CD43, CD99, TdT, PAX-5, BCL-2 and Ki67 in paraffin samples from 38 cases of T-LBL/ALL were detected by immunohistochemical labeling; the miR-16 expression level was detected by real-time RT-PCR. Fifteen cases of reactive hyperplasia of lymph nodes were selected as control. The results indicated that among 38 cases of T-LBL/ALL the positive rate of TdT was highest (94.7%), the positive rate of CD34 was lowest (22.1%), the PAX-5 and CD20 were found to be negative. The Ki67 expression level in 39.5% cases exceeded 80%. As compared with reactive hyperplasia of lymph node, the miR-16 expression in T-LBL/ALL was up-regulated, ant its expression level was 4.87-fold of reactive hyperplasia of lymph node (P < 0.05). The overall survival rate in group of miR-16 high expression decreased (P < 0.05). The prognosis of T-LBL/ALL patients with BCL-2 positive expression was better than that of patients with BCL-2 negative expression (P < 0.05). The miR-16 expression correlated with BCL-2 protein (r = 0.51, P < 0.05). It is concluded that the overall survival rate in miR-16 high expression group is higher than that in miR-16 low expression group, suggesting possible relation of miR-16 with prognosis. Moreover, the prognosis in BCL-2 positive expression group is better than that in negative expression group, which may be a factor influencing prognosis.

[Expression of blood Th17 and CD4(+) CD25(+) Treg cells in patients with aplastic anemia].

This study was aimed to investigate the expression of blood Th17 and CD4(+) CD25(+) regulatory T cells (Treg) in the patients with aplastic anemia (AA). Forty-five patients with AA were enrolled into this study, and were divided into mild aplastic anemia (MAA) group (n = 25) and severe aplastic anemia group (SAA) (n = 20), blood cell count was recorded. 15 healthy donors were enrolled as control. Proportions of blood Th17 and CD4(+) CD25(+) Treg cells were determined by flow cytometry. The serum levels of IL-17, IFN-γ and TNF-α, as well as their concentrations in culture supernatant of phytohemagglutinin (PHA) -stimulated peripheral blood mononuclear cells, were measured by ELISA. The results showed that the proportions of blood Th17 cells and concentration of blood serum IL-17 and IFN-γ increased in patients with SAA, compared with MAA and normal controls, but CD4(+) CD25(+) Foxp3(+) Treg cells obviously decreased in patients with SAA. The concentrations of IL-17 and IFN-γ significantly increased in culture supernatant of SAA group. Hemoglobin level in the patients with AA negatively correlated with the population of Th17 cells and serum IL-17 level, whereas positively correlated with the expression of CD4(+) CD25(+)Treg cells. It is concluded that the increased response of Th17 cells and deficiency of CD4(+) CD25(+) Treg cells present in severe aplastic anemia. The severity of anemia may be related with the imbalance between Th17 and CD4(+) CD25(+)Treg cell response.

[The Effects of IFN-γ on AKT activated 32D Cells and its Mechanisms].

OBJECTIVE: To investigate the effects of activated AKT on murine myeloid precursor cells (32D cells), and the effects of IFN-γ on 32D cells and its mechanisms. METHODS: Plasmid transduction was used to enhance the expression of AKT on 32D cells. After the transfected cells treated with IFN-γ for 24 hours, proliferation rate was tested by WST-1, apoptosis by flow cytometry, expression of phosphorylated Erk1/2, Stat3 and phosphorylated Stat3 was determined by Western blot. RESULTS: (1) IFN-γ at low concentration (100 U/ml) enhanced the growth and proliferation of 32D cells, while at high concentration (1000 U/ml) suppressed them. (2) Compared with control groups, low concentration IFN-γ increased (1124 ± 13) Stat3 phosphorylation in 32D-cell, while it high concentration IFN-γ decreased (601 ± 13). 32D cells transfected with activated Akt grew rapidly (0.287 ± 0.010) and had a low apoptotic rate [(9.57 ± 0.17)% (P < 0.05)]. (3) The expression of p-Erk1/2 in transfected 32D-cell was significantly reduced (P < 0.05). (4) Apoptosis rate of IFN-γ treated group was significantly decreased in transfected 32D cells (P < 0.05). CONCLUSIONS: IFN-γ has dual effects on 32D cells, namely, at low concentration enhanced the growth and proliferation of 32D cells, while at high concentration suppressed them. Its mechanisims is possibly through Stat3 pathway. Activated Akt can significantly promote the growth and proliferation of 32D cell and significantly inhibit apoptosis and IFN-γ can regulate cell proliferation and apoptosis through AKT. AKT activation can inhibit the Erk signal pathway, which may be affected by inhibition the modificaton of Raf1.