同种异体NK细胞对AML细胞体外杀伤活性及初步机制

目的探讨同种异体自然杀伤细胞(NK细胞)对急性髓系白血病(AML)细胞株KG1a的杀伤活性及其分子机制。方法以NK敏感的K562细胞株为对照,免疫磁珠法分离5例健康志愿者NK细胞,乳酸脱氢酶(LDH)释放法测定在不同效靶比时NK细胞对KG1a细胞的杀伤活性,并用流式细胞仪检测KG1a细胞表面人类白细胞抗原I(HLA-I)类分子和NKG2D的配体主要组织相容性复合体(MIC)A/B、ULBP1-3的表达情况。结果效靶比1∶1、5∶1、10∶1、20∶1时NK细胞杀伤K562和KG1a细胞的活性不同,NK细胞对KG1a细胞的杀伤活性较K562细胞明显减低(P<0.01);K562细胞低表达HLA-I类分子,高表达NKG2D配体MIC可溶性Ⅰ类分子相关蛋白A(MICA)、MICA有亲源性的蛋白(MICB)、ULBP1、ULBP2、ULBP3,而KG1a细胞高表达HLA-I类分子,低表达NKG2D配体MICA、MICB、ULBP1、ULBP2、ULBP3。结论同种异体NK细胞对AML细胞株KG1a的杀伤率低于K562细胞;其杀伤率不同的分子基础与其分子表面配体表达差异和HLA-I分子表达率不同有关。

Cytotoxicity of allogenetic natural killer cells against AML cells and molecular mechanism

Objeetive To observe the cytotoxicity of allogenetic natural killer cellsagainst human acute myelocytic leukemia（AML） KGla cell line and its molecular mechanism.Methods The natural killer（NK） cells were isolated from 5 healthy individuals using magnetic cell sorting.The inhibitory effects of cytotoxicity of allogenetic NK cells against human acute myelogenous leukemia KGla cell line were measured by LDH re-lease assay.The expression of natural killer group 2 member D（NKG2D） ligauds（MICA/B,ULBP1,ULBP2,and ULBP3） and human leukocyte antigen（HLA） class I molecules on KG1a cells were assayed by flow cytometery.Results The inhibited the growth rate of KG1a vary with differ-ent effector-to-target.Conclusion NK cells inhibits the growth of KGla cells and up-regulated the expression of NKG2D ligands,and en-hances the sensitivity of KG1 cells to the cytotoxicity of NK cells.