阿霉素增强CIK细胞抗多发性骨髓瘤细胞的机制研究  被引量:1

Mechanism of adriamycin enhanced CIK cells cytotoxicity against multiple myeloma cells

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作  者:姚阳[1] 周民[2] 卢绪章[3] 姜玉[3] 岑岭[3] 张修文[3] 杨建和[3] 

机构地区:[1]泰州职业技术学院,江苏泰州225300 [2]常州市第三人民医院,江苏常州213000 [3]南京医科大学附属常州第二人民医院,江苏常州213000

出  处:《东南大学学报(医学版)》2017年第1期20-23,共4页Journal of Southeast University(Medical Science Edition)

基  金:2014年泰州市科技支撑社会发展计划(指导性)项目(201433);常州市卫生局青年科技项目(QN201203);常州市卫生局重大项目(ZD201311)

摘  要:目的:探讨阿霉素增强细胞因子诱导的杀伤性(CIK)细胞抗多发性骨髓瘤细胞的机制。方法:用阿霉素处理骨髓瘤细胞株U266以及患者骨髓瘤细胞,流式细胞仪(FCM)检测细胞表面NKG2D配体(MICA/B和ULBPs)表达的变化及CIK细胞对U266细胞杀伤作用的变化。结果:阿霉素处理后U266细胞表面MICA/B表达明显升高(P=0.002),而ULBPs的表达无明显变化。阿霉素亦能够诱导患者骨髓瘤细胞表面MICA/B的表达增加。CIK细胞对阿霉素处理过的U266细胞杀伤作用明显增加(P=0.01),这种杀伤作用可以被抗NKG2D抗体部分抑制(P=0.03)。结论:化疗药物诱导骨髓瘤细胞表面MICA/B表达的增加,从而增强CIK细胞对骨髓瘤细胞的杀伤作用。Objective: To explore the mechanism of adriamycin enhanced CIK cells cytotoxicity against multiple myeloma cells. Methods: Multiple myeloma cell line U266 and the cells from patients with multiple myeloma were treated with adriamycin,the expression of NKG2D ligands (MICA/B and ULBPs) were analyzed by flow cytometry (FCM). The cytotoxicity of CIK cells against U266 cell was detected by flow cytometry. Results: The expression of MICA/B on multiple myeloma cell line U266 was up- expression of ULBPs had no changed. The expression regulated after treated with adriamycin ( P = 0. 002), however of MICA/B on primary plasma cells was also up-regulated af- ter treated with adrimycin. The cytotoxicity of CIK cell against U266 was significantly increased by treated with adri- amycin ( P = 0.01 ), and the enhancing cytotoxicity was partly blocked by anti- NKG2D Abs ( P = 0.03 ). Conclu- sion :The cytotoxicity of CIK cells against multiple myeloma an enhance by treated with adriamycin through Up-reg- ulating of MICA/B.

关 键 词:NKG2D配体 细胞因子诱导的杀伤性细胞 骨髓瘤细胞 

分 类 号:R329.2[医药卫生—人体解剖和组织胚胎学]

 

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