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目的:探讨γ-干扰素(IFN-γ)对白血病细胞Fas/FasL表达的调控及凋亡的影响。方法:应用免疫组织化学方法、TUNEL测凋亡法、细胞培养技术,检测人髓系白血病细胞株HL-60及临床髓系白血病患者单个核细胞的Fas的表达及相关功能,并研究γ-干扰素对之的影响。结果:白血病细胞表达Fas蛋白较正常骨髓细胞低,并能致共同培养的Jurkat细胞发生凋亡;而IFN-γ能提高其Fas蛋白的表达(P<0.01),且调节作用具有时间、剂量依赖性,并有下调白血病细胞致Jurkat细胞凋亡的能力,且能够增强白血病细胞对Fas途径介导的凋亡敏感性及增强对化疗药物阿糖胞苷的敏感性。结论:IFN-γ能通过对白血病细胞Fas/FasL系统的调控以防止其逃避免疫监视,并能增强白血病细胞对以Fas/FasL为靶标的化疗药物的敏感性。
Objective: To investigate the effect of IFN-γ on the regulation of Fas / FasL expression and apoptosis in leukemia cells. Methods: The expression of Fas in mononuclear cells of human myeloid leukemia cell line HL-60 and clinical myeloid leukemia was detected by immunohistochemistry, TUNEL assay and cell culture technique. The effects of γ-interference Impact on the right. Results: The expression of Fas protein in leukemia cells was lower than that in normal bone marrow cells and could induce apoptosis in Jurkat cells co-cultured with IFN-γ. IFN-γ increased the expression of Fas protein (P <0.01), and the time-and dose- It also has the ability to down-regulate the apoptosis of Jurkat cells induced by leukemia cells, enhance the sensitivity of leukemic cells to Fas pathway-mediated apoptosis and enhance the sensitivity to chemotherapeutic drug cytarabine. CONCLUSION: IFN-γ can prevent leukemia cells from escaping from immune surveillance by regulating the Fas / FasL system of leukemia cells and enhance the sensitivity of leukemia cells to chemotherapeutic drugs targeting Fas / FasL.