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• 基础研究 • 上一篇    下一篇

NK细胞与K562细胞之间相互免疫编辑作用及其对NK细胞杀伤活性的影响

郭坤元1,2,梅家转1,姜振宇3,姚开泰2   

  1. (1.南方医科大学珠江医院血液科,广东 广州 510282;2.南方医科大学基础医学院病理学教研室,广东 广州 510515;3.吉林大学第一医院血液肿瘤科,吉林 长春130021)
  • 收稿日期:2007-01-09 修回日期:1900-01-01 出版日期:2007-07-28 发布日期:2007-07-28
  • 通讯作者: 姚开泰

Reciprocal immunoediting between NK cells and K562 cells and its effect on NK cell-mediated cytotoxicity

GUO Kun-yuan1, 2, MEI Jia-zhuan1, JIANG Zhen-yu3, YAO Kai-tai2   

  1. 1. Department of Hematology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China;2. Department of Pathology, School of Basic Medical Sciences,Southern Medical University, Guangzhou 510515, China;3. Department of Hematology and Oncology, First Hospital, Jilin University, Changchun 130021, China
  • Received:2007-01-09 Revised:1900-01-01 Online:2007-07-28 Published:2007-07-28
  • Contact: YAO Kai-tai

摘要: 目的:探讨NK细胞与K562细胞混合培养前、后其杀伤活性的变化及分子机制。方法:流式细胞仪检测NK细胞与K562细胞混合培养前、后细胞表面相应分子的变化,LDH释放法测定效靶比20∶1时NK细胞对K562细胞的杀伤活性。结果:相互编辑前,K562细胞表面MICA/MICB的表达率为(79.90±0.87)%,NK细胞表面NKG2D、KIR2DL1和KIR3DL1的表达率分别为(98.27±0.67)%、(45.70±1.22)%和(35.60± 1.35)%。相互编辑后,K562细胞表面MICA/MICB和NK细胞表面NKG2D的表达率分别为(35.56±1.01)和(34.67±3.88)%,均明显低于编辑前(P=0.000);NK细胞表面KIR2DL1和KIR3DL1的表达率分别为(47.20±1.08)%和(34.03±1.20)%,与编辑前比较差异均无显著性(P>0.05)。效靶比20∶1时,NK细胞对编辑后的K562细胞的杀伤活性为(24.07±0.58)%,编辑后的NK细胞对K562细胞的杀伤活性为(16.95±2.00)%,均明显低于编辑前NK细胞对K562细胞的杀伤活性[(54.03±3.46)%](P=0.000)。结论: NK细胞与K562细胞持续性接触后,双方发生了相互免疫编辑作用;NK细胞的杀伤活性下降,其分子机制是细胞表面相应的配受体发生了变化。

关键词: 杀伤细胞, 天然, NKG2D, MHC I 类链相关分子, 免疫编辑

Abstract: To analyze the changes of cytotoxicity mediated by NK cells after 24 h coculture with K562 cells and the molecular mechanism. Methods The expressions of MICA/MICB on K562 cells, KIR2DL1, KIR3DL1, NKG2D on NK cells were analyzed by flow cytometry. Cytotoxicity was detected by LDH releasing assay. Results Before editing,the expression rate of MICA/MICB on K562 cells was (79.90±0.87)%, the expression rates of NKG2D,KIRZDL1, and KIR3DL1 on NK cells were (98.27±0.67)%, (45.70±1.22)% and (35.60±1.35)%,respectively.After editing,the expression rates of M1CA/M1CB on K562 cells and NKG2D on NK cells were (35.56±1.01)% and (34.67±3.88)%,respectively;compared with before editing,there was significant difference(P=0.000).The expression rates of KIR2DL1 and KIR3DL1 on NK cells were (47.20±1.08)% and (34.03±1.20)%,compared with before editing,there was no signficant difference(P>0.05).The cytotoxicities against K562 cells by edited NK cells and against the edited K562 cells by NK cells were(24.07± 0.58)% and (16.95±2.00)% at an effector-to-target (E/T) ratio of 20∶1, both were lower than the cytotoxicity against K562 cells by NK cells (54.03%±3.46%), the differences weresignificant (P=0.000). Conclusion Reciprocal immunoediting between NK cells and K562 cells induced by 24 h coculture leads to decreased cytotoxicity of NK cells. The potential molecular mechanism is the changes of NKG2D and MICA/MICB expressions.

Key words: killer cells, natural, NKG2D, MHC class I chain related molecules, immunoediting

中图分类号: 

  • R392.12