体外诱导白血病源性树突状细胞及其对T细胞杀伤活性影响的研究  

Induction of leukemic dendritic cells in vitro and study of cytotoxic activity against chronic myelogenous leukemia cells generated by dendritic cells-stimulated autologous T cells

在线阅读下载全文

作  者:张滔[1] 常瑛[1] 

机构地区:[1]首都医科大学附属北京友谊医院血液科,北京100050

出  处:《临床血液学杂志》2003年第2期76-78,共3页Journal of Clinical Hematology

摘  要:目的 :探讨体外培养白血病源性树突状细胞 (DC)及其对T细胞杀伤活性的影响。方法 :从慢性髓细胞性白血病 (CML)患者外周血中分离单个核细胞 ,加入 1× 10 6U/L粒 巨噬细胞集落刺激因子 (GM CSF)、1×10 6U/L白细胞介素 (IL) 4和 5 0× 10 3 U/L肿瘤坏死因子 (TNF α) ,每 3~ 4天换液 1次 ,连续培养 14天 ,获得DC。取外周血单个核细胞加入 5 0 0× 10 3 U/LIL 2 ,培养至第 7天 ,把细胞分成两组 ,其中一组加入培养的DC ,两组细胞继续培养 3~ 4天 ,然后测定T细胞杀伤活性。结果 :DC具有典型的树状突起 ,高表达CD1a,具有慢粒特异性染色体t(9;2 2 ) ,能增强T细胞对白血病细胞的杀伤活性。结论 :在体外利用细胞因子可以把CML细胞诱导分化成具有刺激T细胞产生细胞毒性反应的白血病源性DC。Objective:To generate Dendritic Cells (DC) from peripheral blood monocyte cells (PBMNCs) of patients with Chronic Mylogenous Leukemia (CML) in vitro and study cytotoxic activities against CML cells caused by T cells stimulated with leukemic DC and interleukin 2.Method:We generated DC from PBMNCs of CML that incubated concurrently with granulocyte macrophage colony stimulating factor (GM CSF) 1000u/ml, interleukin 4 (IL 4) 1000u/ml and tumor necrosis factor α (TNF α) 50u/ml for 14 days. PBMNCs of CML were cultured with IL 2 500 μ/ml for 7 days and divided into two groups. We added DC into one of groups and mensurated cytotoxic activities of two groups after 3 4days.Result:these cells had typical dendritic morphology, express high levels of CD 1a .Analysis of chromosome showed the presence of t (9; 22) in the nuclei of these cells.T cells stimulated with leukemic DC and interleukin 2 show strong cytotoxic responses against leukemic cells.Conclusion:cytokine driven in vitro differentiation of CML cells results in generation of DC with potent T cell stimulatory funtion.

关 键 词:树突状细胞 慢性白血病 髓细胞性 细胞活性 T细胞 

分 类 号:R733.7[医药卫生—肿瘤]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象