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目的:探索急性髓细胞白血病(AML)骨髓中Th17细胞及其相关因子在AML发生与发展中的作用。方法:选取初诊AML患者23例,另取25名健康志愿者为对照。采用流式细胞仪分别测初诊AML组、初诊AML组诱导缓解后、对照组骨髓中CD3~+ CD161~+ IL-17~+ IFN-γ~+ T细胞的比例。采用ELISA法检测初诊AML组、初诊AML组诱导缓解后、对照组骨髓液中血管内皮生长因子(VEGF)、IL-17浓度;对VEGF与IL-17进行相关性分析。结果:初诊AML组骨髓中CD3~+ CD161~+ IL-17~+ IFN-γ~+ T细胞的比例为(1.52±0.10)%,初诊AML组诱导缓解后CD3~+ CD161~+ IL-17~+ IFN-γ~+ T细胞的比例为(1.36±0.06)%,对照组骨髓中CD3~+ CD161~+ IL-17~+ IFN-γ~+ T细胞的比例为(0.22±0.04)%。初诊AML组VEGF浓度(254.08±24.34)pg/ml,IL-17浓度(20.24±3.82)pg/ml;初诊AML组诱导缓解后VEGF浓度(137.37±22.51)pg/ml,IL-17浓度(10.42±2.96)pg/ml;对照组骨髓液中VEGF浓度(125.98±14.96)pg/ml,IL-17浓度(10.59±2.87)pg/ml;VEGF与IL-17呈正相关。结论:Th17细胞具有促进AML发生与发展的作用。
Objective: To explore the role of Th17 cells and related factors in the development and progression of AML in acute myeloid leukemia (AML). Methods: Twenty-three newly diagnosed AML patients and 25 healthy volunteers were selected as controls. The proportions of CD3 ~ + CD161 ~ + IL-17 ~ + IFN-γ ~ + T cells in the bone marrow of the control group after induction of remission were determined by flow cytometry in the newly diagnosed AML group and newly diagnosed AML group. The concentrations of vascular endothelial growth factor (VEGF) and IL-17 in bone marrow fluid of the newly diagnosed AML group and newly diagnosed AML group were detected by ELISA. The correlation between VEGF and IL-17 was analyzed. Results: The proportion of CD3 ~ + CD161 ~ + IL-17 ~ + IFN-γ ~ + T cells in the newly diagnosed AML group was (1.52 ± 0.10)%, the CD3 ~ + CD161 ~ + IL-17 The proportion of CD3 ~ + CD161 ~ + IL-17 ~ + IFN-γ ~ + T cells in control group was (0.22 ± 0.04)% . The newly diagnosed AML group had VEGF concentration of (254.08 ± 24.34) pg / ml and IL-17 concentration of 20.24 ± 3.82 pg / ml, VEGF concentration of newly diagnosed AML group (137.37 ± 22.51) pg / ml and IL- ± 2.96) pg / ml; VEGF concentration in control group was (125.98 ± 14.96) pg / ml and IL-17 concentration was (10.59 ± 2.87) pg / ml; VEGF and IL-17 were positively correlated. Conclusion: Th17 cells can promote the occurrence and development of AML.