郑述凌 张叔人 王冬梅 马文波 周春霞 曲平 张友会 100021 北京，中国医学科学院中国协和医科大学肿瘤研究所肿瘤医院 中华肿瘤杂志 1998 0 0 5


    关键词：非免疫原性肿瘤 B7-1基因 干扰素-γ 基因表达 基因，MHC I类 期刊 zhzlzz 0 基础研究 fur -->


    

【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MHC I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MHC I分子的表达，两者可协同发挥作用，诱发肿瘤排斥。

    Rejection of non-immunogenic tumor cells transfected with costimulatory molecule B7 after treatment with IFN-γ in vitro Zheng Shuling, Zhang Shuren, Wang Dongmei, et al. Cancer Institute(Hospital), Chinese Academy of medical Sciences, Peking Union Medical College, Beijing 100021

    【Abstract】 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.

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