IL－2和TNF特异性基因治疗后肝癌组织病理及免疫组化分析

Pathological and immunohistochemical analyses of the tumor bodies following the treatment with the hepatoma-specific interleukin-2 and tumor necrosis factor gene therapy

目的：探讨ＴＮＦ和ＩＬ－２基因治疗后实验性肝癌瘤体内细胞水平的改变。方法：应用病理检查和免疫组化分析对ＩＬ－２和ＴＮＦ转基因治疗后的实验性肝癌病理改变及免疫细胞浸润进行分析。结果：发现受白蛋白增强子／启动子转录调控的ＩＬ－２和ＴＮＦ基因在原位感染实验性肝癌可使肝癌逐渐缩小。ＴＮＦ基因可使肝癌组织内广泛出血坏死，Ｍａｃ－１＋炎细胞浸润为主；ＩＬ－２基因可使肝癌组织内大片坏死，Ｌｙｔ２＋炎细胞浸润，两组治疗后期均出现明显的纤维化。结论：ＩＬ－２或ＴＮＦ肝癌特异性原位基因治疗介导免疫抗肿瘤反应，但机理有所不同。

To detect cellular variation in the experimental hepatoma bodies following in situ interleukin-2(IL-2) and tumor necrosis factor(TNF) gene therapy in the tissue-specific manner. Methods:Pathological and immunohistochemical analyses were employed to detect the pathological variation and infiltration of immune cells in the hepatoma following the treatment with IL-2 and TNF gene transfer. Results: It was found that the hepatoma regressed gradually following in situ transfer with IL-2 and TNF genes under transcriptional control of albumin enhancer/promoter. Significant bleeding, necrosis and massive infiltration of Mac-1+ inflammatory cells in the hepatoma tissues were found after TNF gene therapy.Massive necrosis. infiltration of Lyt2+ inflammatory cells in the hepatoma tissues were apparent after IL-2 gene therapy. Fibrosis was significant at late stage of the treatment eithet with IL-2 or with TNF gene transfer. Conclusion: In situ hepatoma-specific gene therapy with IL-2 and TNF gene mediates anti-hepatoma immune response, but the mechanisms seem different.