B7基因转导非免疫原性肿瘤B16并联合应用IFN-γ的抗肿瘤研究  

Rejection of non immunogenic tumor cells transfected with costimulatory molecule B7 after treatment with IFN γ in vitro

作　　者：郑述凌[1] 张叔人[1] 王冬梅[1] 马文波[1] 周春霞[1] 曲平[1] 张友会[1] 

机构地区：[1]中国医学科学院中国协和医科大学肿瘤研究所肿瘤医院

出　　处：《中华肿瘤杂志》1998年第5期333-336,共4页Chinese Journal of Oncology

摘　　要：目的探索非免疫原性肿瘤的免疫基因治疗。方法将Ｂ７１基因导入非免疫原性肿瘤细胞Ｂ１６，在体外经ＩＦＮγ处理后，观察细胞表面分子的表达变化，以及肿瘤细胞在小鼠体内的成瘤性。结果单独Ｂ７基因转导的Ｂ７＋Ｂ１６在小鼠体内持续生长。体外用ＩＦＮγ处理肿瘤细胞，可明显增加细胞表面ＭＨＣＩ类分子的表达，与Ｂ７－Ｂ１６比较，Ｂ７＋Ｂ１６在小鼠体内的成瘤性明显降低。结论单独Ｂ７基因导入并表达，不能改变Ｂ１６在体内恶性增殖的特性。同时提高细胞表面Ｂ７与ＭＨＣＩ分子的表达，两者可协同发挥作用，诱发肿瘤排斥。Objective To explore immuno gene therapy of non immunogenic tumor. Methods Non immurogenic tumor cells B16 were transfected with B7 1 gene. The B7 1 gene transfected B16 cells (B7 +B16) were treated with recombinant murine interferon gamma (rmIFN γ) in vitro, and then inoculated to C57BL/6 mice. Results While B7 +B16 cells grew progressively in syngeneic mice, tumorigenicty was significantly reduced when B7 +B16 cells were treated with rmIFN γ before inoculation to mice. Flow cytometric analysis of the rmIFN γ treated B7 +B16 cells showed significant up regulation of MHC classⅠexpression. Conclusion For non immunogenic tumor if the expressions of MHC class I molecules is low, providing co stimulatory molecule B7 is not enough to reduce tumorigenicity. The B7 1 gene transfected B16 cells become non tumorigenic or weakly tumorigenic when their MHC class I is up regulated.

关 键 词：肿瘤 非免疫原性肿瘤 B7-1基因 干扰素γ 

分 类 号：R73－36[医药卫生—肿瘤] R730.5[医药卫生—临床医学]