摘要
目的:观察AS2O3对CD34+早期急性髓系白血病细胞NKG2D配体表达及NK细胞杀伤活性的影响。方法:流式细胞仪检测KG1a细胞表面CD34抗原表达率,MTT法确定AS2O3的基本工作浓度,以不同浓度的AS2O3处理KG1a细胞,流式细胞仪测定处理前后KG1a细胞NKG2D配体的表达情况;MACS法分离5例健康个体的NK细胞,LDH释放法检测NK细胞对AS2O3处理前后KG1a细胞的杀伤活性。结果:10nmol/ml的AS2O3作用KG1a细胞后,能使KG1a细胞表面ULBP1的表达水平显著上调(P<0.05),同时也激发了NK细胞对KG1a细胞的杀伤活性(P<0.05)。结论:AS2O3能上调CD34+白血病细胞表面NKG2D配体的表达水平,诱导NK细胞对其的杀伤活性,启示AS2O3可与NK细胞组成过继性免疫化疗方案,提高急性白血病的疗效。
Objective： To explore the effects of arsenic trioxide （As2O3） on expression of NKG2D ligands on the surface of CD34^＋ AML cells and its impact on normal NK cytotoxicity. Methods： Expression of CD34 antigen on KGla cells, a cell line of acute myelogenous leukemia （AML） ,was detected by FACS. KGla cells were treated by AS2O3 in different concentrations, then expression of NKG2D ligands on the cells was observed with FACS. NK cells were isolated from 5 healthy persons with MACS and their cytotoxicity was detected by LDH releasing assay. Results：Expression of ULBP1 on KGla cells was increased when incubated with 10 nmol/ml of AS2O3（ P 〈 0.05）. Cytotoxicity of NK cells from normal individuals against the AS2O3-treated KGla cells was enhanced significantly（ P 〈 0.05）. Conclusion： AS2O3 increases the expression of NKG2D ligands on CD34 ^＋ leukemia cells, which induces enhanced NK cytotoxicity.
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2008年第6期509-511,517,共4页
Chinese Journal of Immunology
基金
国家自然科学基金资助项目(30471636)
