Objective:To investigate the effects of soluble factors secreted by acute myeloid leukemia(AML) cells on the phenotypical and functional properties of DCs derived from normal mononuclear cells. Methods:Mononuclear cells were cul-tured with interleukin-4(IL-4) and granulocyte-macrophage colony-stimulating factor(GM-CSF),in the presence or absence of 24 h culture supernatants from fresh primary AML cells,to generate immature DCs. The maturation of DCs was induced by cytokines IL-1beta,IL-6,tumor necrosis factor-alpha(TNF-alpha),and prostaglandin-2(PGE-2). The phenotypic alterations of DCs and DCs-primed CD4+ T cells were evaluated using flow cytometry. Precursor frequency(PF) was calculated to monitor the allostimulatory effects of DCs on CD4+ and CD8+ T cells. Results:AML cell supernatant-treated DCs showed significantly lower expression of co-stimulatory molecules CD80 and CD86,and reduced response to cytokines IL-1beta,IL-6,TNF-alpha,and PGE-2. The allostimulatory effects of AML cell supernatant-treated DCs on CD4+ and CD8+ T cells were significantly lower than those of normal mature DCs [PF:(1.8 ± 0.5)% vs.(5.2 ± 1.6)% for CD4+ T cells,(2.1 ± 0.6)% vs.(6.5 ± 2.0)% for CD8+ T cells,P < 0.01]. These AML supernatant-induced DCs could also induce allogeneic CD4+ T cells to differentiate into CD4+CD25high T cells,which had immunophenotyping characteristics of regulatory T cells,i.e. they expressed Foxp3 but not active maker CD69. Conclusion:This study demonstrates that soluble factors secreted by AML cells can inhibit development and functions of DCs. In addition,AML supernatant-induced DCs can induce the generation of CD4+CD25high T cells from CD4+ T cells,which may be a mechanism of increased prevalence of CD4+CD25high regulatory T cells and immune dysfunction in AML patients. Objective: To investigate the effects of soluble factors secreted by acute myeloid leukemia (AML) cells on the phenotypical and functional properties of DCs derived from normal mononuclear cells. Methods: Mononuclear cells were cul-tured with interleukin-4 (IL- The presence of or absence of 24 h culture supernatants from fresh primary AML cells, to generate immature DCs. The maturation of DCs was induced by cytokines IL-1 beta, IL-6, The phenotypic alterations of DCs and DCs-primed CD4 + T cells were evaluated using flow cytometry. Precursor frequency (PF) was calculated to monitor the allostimulatory effects of DCs on CD4 + and CD8 + T cells. Results: AML cell supernatant-treated DCs showed significantly lower expression of co-stimulatory molecules CD80 and CD86, and reduced response to cytokines IL-1beta, IL-6, TNF- alpha, and PGE -2. The allostimulatory effects of AML cell supernatant-treated DCs on CD4 + and CD8 + T cells were significantly lower than those of normal mature DCs [PF: (1.8 ± 0.5)% vs. (5.2 ± 1.6)% for CD4 + T cells, (2.1 ± 0.6)% vs. 6.5 ± 2.0)% for CD8 + T cells, P <0.01]. These AML supernatant-induced DCs could also induce allogeneic CD4 + T cells to differentiate into CD4 + CD25 high T cells, which had immunophenotyping characteristics of regulatory T cells, ie they expressed Foxp3 but not active maker CD69. Conclusion: This study demonstrates that soluble factors secreted by AML cells can inhibit development and functions of DCs. In addition, AML supernatant-induced DCs can induce the generation of CD4 + CD25high T cells from CD4 + T cells, which may be a mechanism of increased prevalence of CD4 + CD25 high regulatory T cells and immune dysfunction in AML patients.