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

机译:FasL / B7-1基因诱导的抗食管癌积极免疫改性肿瘤细胞

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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{sup}+/B7-1{sup}+ 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:为了研究FasL / B7-1(FB-11)基因改性肿瘤细胞诱导的食管癌细胞CTL的激活,并探讨了ECA-109肿瘤细胞中FASL和B7-1的共同表达是否可以启动协同效应抗肿瘤效应。将FasL和B7-1基因与腺病毒载体转染到人体ECA-109 ECA-109癌细胞中。通过G418选择阳性克隆。通过流式细胞术和RT-PCR检测FasL和B7-1。从用ECA-109 / FB-11或腹膜型ECA-109细胞免疫的小鼠获得腹渗透淋巴细胞和敏化脾细胞,并且通过MTT测定法测定这些CTL对肿瘤细胞的细胞毒性。流式细胞术和RT-PCR显示出高度表达FasL和B7-1。 FasL {sup} + / b7-1 {sup} + eCa-109细胞(ECA-109 / FB-11)皮下皮下接种在C57BL / 6小鼠的背部皮肤中,然后大大降低致瘤性(Z = 2.15- 46.10,P <0.01)。 ECA-109 / FB-11细胞致敏小鼠对野生型ECA-109细胞的重新进行(Z = 2.06-44.30,P <0.05)获得了保护性免疫活性。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细胞活化的CTLS(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CTL对食管癌细胞的活性。

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