CCR5受体参与CIK细胞穿过人脑微血管内皮细胞单层的过程  

CIK cells through the CCR5 receptor through the research of human brain microvascular endothelial cells monolayer

作　　者：马英桓[1] 孙岩[1] 李东文[1] 

机构地区：[1]中国人民解放军第四六三医院肿瘤科,辽宁沈阳110042

出　　处：《现代肿瘤医学》2017年第19期3046-3049,共4页Journal of Modern Oncology

基　　金：国家自然科学基金青年基金项目(编号:81300452);辽宁省自然基金(编号:2014020167)

摘　　要：目的:选用高表达MIP-1α的人CIK细胞作为模式细胞对穿过人脑微血管内皮细胞单层机制进行探讨。方法:通过应用蛋白免疫印迹技术、真核表达载体的构建与细胞转染技术,同时进行跨内皮迁移和抗体封闭实验,集中探讨HBMEC膜受体趋化因子受体5(CCR5)在CIK细胞穿过HBMEC单层过程中的作用。结果:在CIK细胞与HBMEC单层单独孵育过程中,引起HBMEC膜受体CCR5表达变化;HBMEC膜受体CCR5的高表达使Jurkat细胞穿过HBMEC单层能力增强。结论:HBMEC膜受体CCR5参与了CIK细胞穿过HBMEC单层过程。Objective：To select high expression of MIP - 1 as a model of alpha CIK cells to through the mecha- nism of human brain microvascular endothelial cells monolayer were discussed. Methods ： In the present stmty, CIK cells were used as a model of human T - cell acute lymphoblastie leukemia to investigate the role of CCR5 in the progess of the transendothelial migration of T cells. Western blot, plasmid construction and transfection, transendothelial migration and endothelial permeability assay are used to explore the progress of the transendothelial migration of T ceils. Results：MIP - 1α induced the expression of CCR5, a potential MIP - 1α receptor,on HBMECs. HBMECs tranfected with CCR5 resulted in increased CIK cells transendothelial migration. CCR5 antagonist （2D7 mAb） blocked the CIK cells transmigration. The induced expressions of CCR5 could involve the migration of CIK cells through HB- MECs monolayer. Conclusion：MIP - 1 c~ levels in CIK cells and its receptor CCR5 appeared to be an import factor fbr its transendothelial migration,which may provide the theoretical basis to understand the mechanisms of brain metastases of human acute lymphoblastic leukemia T - cells at cellular and molecular levels.

关 键 词：趋化因子受体5 人CIK细胞系 人脑微血管内皮细胞 

分 类 号：R73-3[医药卫生—肿瘤] R329.28[医药卫生—临床医学]