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Anti- esophageal cancer active immunity induced by FasL/B7-1 genes modified tumor cells

机译:FasL / B7-1基因修饰的肿瘤细胞诱导的抗食道癌主动免疫

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To study the activation of CTLs against esophageal cancer cells induced by FasL/B7-1 (FB-11)genes modified tumor cells, and to explore whether co-expression of FasL and B7-1 in Eca-109 tumor cells could initiate an synergistic antitumor effect. FasL and B7-1 genes were transfected into human Eca-109 Eca-109 cancer cells with adenovirus vectors. The positive clones were selected by G418. FasL and B7-1 were detected by Flow cytometry and RT-PCR. The abdominal infiltrating lymphocytes and sensitized spleen cells were obtained from the mice who were immunized with Eca-109/FB-11 or wild type Eca-109 cells intraperitoneally, and the cytotoxicity of these CTLs against tumor cells was determined by MTT assay. Flow cytometry and RT-PCR showed that FasL and B7-1 were highly expressed. FasL+/B7-1+ Eca-109 cells (Eca-109/FB-11) were inoculated subcutaneously in the dorsal skin of C57BL/6 mice and then they decreased their tumorigenicity greatly (z=2.15-46.10, p<0.01). The Eca-109/FB-11 cell-sensitized mice obtained the protective immune activity against the rechallenge of wild type Eca-109 cells (z=2.06-44.30, p<0.05). It was showed that the cytotoxicity of CTLs induced by Eca-109/FB-11 cells against Eca-109 was significantly higher than that of CTLs activated by wild-type Eca-109 cells (84.1±2.4% vs 30.5±2.3%, p<0.05). The results suggest that the FasL and B7-1 can effectively promote the activity of CTLs against esophageal cancer cells.
机译:研究由FasL / B7-1(FB-11)基因修饰的肿瘤细胞诱导的食管癌细胞对CTL的激活,并探讨Eca-109肿瘤细胞中FasL和B7-1的共表达是否可以启动协同作用抗肿瘤作用。用腺病毒载体将FasL和B7-1基因转染到人Eca-109 Eca-109癌细胞中。通过G418选择阳性克隆。流式细胞仪和RT-PCR检测FasL和B7-1。从经腹膜内用Eca-109 / FB-11或野生型Eca-109细胞免疫的小鼠获得腹部浸润淋巴细胞和致敏脾细胞,并通过MTT测定确定这些CTL对肿瘤细胞的细胞毒性。流式细胞仪和RT-PCR表明FasL和B7-1高表达。将FasL + / B7-1 + Eca-109细胞(Eca-109 / FB-11)皮下接种到C57BL / 6小鼠的背部皮肤中,然后它们的致瘤性大大降低(z = 2.15-46.10,p <0.01)。 Eca-109 / FB-11细胞致敏的小鼠获得了针对野生型Eca-109细胞再攻击的保护性免疫活性(z = 2.06-44.30,p <0.05)。结果表明,Eca-109 / FB-11细胞诱导的CTL对Eca-109的细胞毒性显着高于野生型Eca-109细胞激活的CTL(84.1±2.4%vs 30.5±2.3%,p <0.05)。结果表明FasL和B7-1可以有效地促进CTLs对食道癌细胞的活性。

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