活化巨噬细胞通过接触导致肿瘤细胞凋亡  

Activated macrophages induce apoptosis in tumor cells through α cell-contact dependent mechanism

作　　者：张领兵[1] 于乐洋[1] 闫东梅[1] 马威[1] 杜柏榕[1] 朱迅[1] 

机构地区：[1]吉林大学基础医学院免疫教研室,长春130021

出　　处：《中国免疫学杂志》2007年第3期240-242,共3页Chinese Journal of Immunology

摘　　要：目的探讨活化巨噬细胞与肿瘤细胞间接触引起肿瘤细胞死亡的机制。方法通过卡介苗体内刺激和脂多糖体外刺激分别获得活化的巨噬细胞,通过体外细胞毒实验,检验其对MCA207肿瘤细胞的杀伤活性;利用流式细胞技术检测巨噬细胞表面Mac-1、TNF-α的表达情况。结果活化的巨噬细胞可以通过与肿瘤细胞接触杀伤肿瘤细胞,这种杀伤活性不受多聚甲醛固定的影响,但胰蛋白酶消化能使杀伤活性丧失;这种杀伤活性是通过诱导肿瘤细胞凋亡实现的,但并不是由细胞表面TNF-α引起的。结论巨噬细胞表面还存在目前未知的效应分子,该分子可以诱导MCA207细胞发生凋亡。Objective ：To explore the mechanism of activated macrophages contact dependent cytotoxicity. Methods： Activated routine peritoneal macrophages were obtained by introperitoncal injection Bacille Calmette Guerin and fixed with 1% paraformaldehyde. Using these fixed activated macrophages as effector cells, an in vitro cytotoxicity assay was conducted with MCA207 as target cells. The expression levels of Mac-1 and TNF-α on macrophages were examined FITC-conjugated Abs using flow cytometric analysis. Results： MCA207 were killed by macrophages in a cell-contact dependent manner through apoptosis. The apoptosis inducing activity was trypsin sensitive and TNF-α independent. Conclusion： There are some novel protein ligands on the membrane of activated macrophages, which can induce tumor cells apoptosis.

关 键 词：巨噬细胞 卡介苗 脂多糖 肿瘤坏死因子 细胞毒活性 凋亡 

分 类 号：R392.12[医药卫生—免疫学]