细胞因子诱导的杀伤细胞可诱导bcr-abl阳性的K562细胞凋亡

表达bcr-abl的K562细胞能抵抗不同化疗药和诱导的细胞凋亡，为了观察细胞因子诱导的杀伤（CIK）细胞能否诱导表达bcr-abl的K562细胞凋亡，应用流式细胞术DNA亚G1期分析法比较CIK和化疗药物（喜树碱和VP－16）诱导K562及CEM细胞发生凋亡的情况，结果表明，RT－PCR检测显示K562细胞表达bcr-abl融合基因mRNA，单独K562细胞对照组，K562／喜树碱组及K562／VP－16组均未见亚G1期峰，K562／CIK组亚G1期峰值为38．1％，单儿CEM细胞对照组未见亚G1期峰，CEM／喜树碱组亚G1期峰值为23．5％，CEM／VP－16组亚G1期峰值为32．3％，CEM／CIK组亚G1期峰值为45．4％。结论：喜树碱和VP－16不能诱导表达bcr-abl的K562细胞凋亡，而CIK细胞能诱导K562细胞凋亡，提示过继细胞免疫治疗可能在CML病人异基因髓移植及移植后淋巴细胞输注中起重要作用。

Cytokine-Induced Killer Cells Induce Apoptosis of K562 Cells Expressed bcr-abl

In order to investigate whether cytokine induced killer(CIK) cells can induce apoptosis of bcr abl + K562 cells, apoptosis of K562 cells and CEM cells induced by CIK cells, etoposide or camptothecin was detected with flow cytometry DNA assay. RT PCR showed that K562 cells expressed the bcr abl fusion gene, K562 cells, K562 cells/etoposide or K562 cells/camptothecin groups showed no sub G 1 peak. K562 cells/CIK cells group showed sub G 1 peak(38.1%). CEM cells showed no sub G 1 peak. CEM cells/camptothecin or CEM cells/etoposide groups showed sub G 1 peak(23.5% or 32.3% respectively). CEM cells/CIK cells group showed sub G 1 peak(45.4%). Etoposide or camptothecin did not induce apoptosis of K562 cells. CIK cells induce apoptosis of K562 cells. Bcr abl fusion gene prevented apoptosis induced by etoposide or camptothecin, but did not prevent apoptosis induced by CIK cells. This property may support the observed adoptive immunologic effect of allogeneic bone marrow transplantation and donor lymphocyte transfusions of CML case relapsing after allogeneic bone marrow transplantation.