摘要
目的观察MUC1/CD3双特异性抗体(BsAb)介导下淋巴因子激活的杀伤细胞(LAK细胞)对过度表达MUC1基因的乳腺癌MCF-7细胞株的杀伤作用。方法化学耦连法制备MUC1/CD3双特异性抗体(BsAb)。显微镜下计数A组(BsAb+MCF-7+LAK)、B组(a-CD3+MCF-7+LAK)、C组(a-MUC1+MCF-7+LAK)、D组(a-CD3+a-MUC1+MCF-7+LAK)及E组(RPMI1640培养基+MCF-7+LAK)LAK-MCF-7细胞数目,并计算LAK细胞与MCF-7细胞的结合率。MTT法检测各组LAK细胞对MCF-7细胞的杀伤率。结果A组MCF-7细胞和LAK细胞的结合率及LAK细胞对MCF-7细胞的杀伤率均明显高于B、C、D、E组(P均<0.05)。结论MUC1/CD3BsAb能显著提高LAK细胞与乳腺癌MCF-7细胞的结合率,并显著提高LAK细胞对乳腺癌MCF-7细胞的杀伤率。
[Objective] To observe the regulatory effects of LAK cells mediated by MUC1/CD3 BsAb on MCF-7 breast cancer ceils in vitro. I-Methods7 MUC1/CD3 BsAb wos established by,chemical conjugating of CD3 McAb and MUC1 McAb. The combination of LAK cells and MCF-7 breast cancer cells was obstrved in A group （BASb＋MCF-7＋LAK）,B group（a-CD3＋MCF-7A-LAK）,C group（a-MUC1＋MCF-7＋LAK）,D group（a-CD3 ＋ a-MUC1＋MCF-7A-LAK）and E group（RPMI1640＋MCF-7＋LAK）. Cytotoxicity of LAK cells to MCF-7 cells was observed by MTT assay.[Results] The combination rate of LAK cells and MCF-7 cells and the cytotoxicity activity of LAK cells against MCF-7 breast cancer cells induced by BsAb were significantly higer than B group,C group ,D group and E group （ P 〈 0. 05）. [Conclusion] BsAb could can ingrease the combination rates of LAK cells and MCF-7 breast cancer cells,and increase the cytotoxicity of LAK cells against MCF-7 breast cancer cells.
出处
《山东医药》
CAS
北大核心
2007年第9期18-19,共2页
Shandong Medical Journal
基金
河北省科技厅科技攻关项目(052761565)
