CD4+CD25+ Regulatory T Cells in Patients with Acute Lymphocytic Leukemia.

Abstract

Human CD4+CD25+ regulatory T (Treg) cells suppress antigen-specific T cell immune response and contribute to peripheral tolerance. However, little is known about the role of Treg cells in the pathogenesis of acute lymphocytic leukemia (ALL). In this study, the proportion of CD4+CD25+ Treg cells in the peripheral blood of three groups of people [the patients with ALL who had never received any chemotherapy before, the patients with ALL who had achieved partial remission (PR) or complete remission (CR) after chemotherapy and the healthy donors] was evaluated by flow cytometry. The expression level of Foxp3 mRNA of each group was examined by real-time RT-PCR. In vitro, the peripheral blood mononuclear cells (PBMC) from healthy donors were cultured in the serum of ALL patients without chemotherapy; each group was divided into sub-groups according to various serum doses. After co-cultured for 72 hours, the cells of all the groups were harvested separately and further tested the number of CD4+CD25+ Treg cells and the mRNA expression of Foxp3. The results showed that both the percentage of CD4+CD25+ T cells and the mRNA expression level of Foxp3 in patients with chemotherapy were significantly higher than those of the healthy donors and patients without chemotherapy (P<0.01 and P<0.01). Although the population of CD4+CD25+ T cells in ALL patients without chemotherapy was almost the same to that in the healthy donors (P>0.05), the expression of Foxp3 mRNA in former was higher (P<0.05) .The serum derived from ALL patients without chemotherapy remarkably increased the proportion of CD4+CD25+ T cells and the expression level of Foxp3 mRNA in co-cultured system, both of which were statistically higher than those in controls (P<0.05 and P<0.01) and did not vary with the serum dose. These results suggest that the chemotherapy may exert an influence on the production of CD4+CD25+ Treg cells and CD4+CD25+ Treg cells may play an important role in the pathogenesis of ALL.