摘要
目的:研究新城疫病毒(Newcastle disease virus,NDV)弱毒株NDV7793能否促进人CD4+T细胞表达肿瘤坏死因子相关凋亡因子诱导配体(TNF-related apoptosis-inducing ligand,TRAIL)。方法:首先用免疫磁珠分选法(magnetic activated cell sorting,MACS)分选外周血静止CD4+T细胞,然后加抗CD3抗体、抗CD28抗体和白细胞介素-2(interleukin-2,IL-2)使之成为能被NDV激活的CD4+T细胞。用流式细胞技术(flow cytometry,FCM)检测NDV刺激的CD4+T细胞的TRAIL的表达水平。结果:MACS法分选外周血得到的CD4+T细胞纯度达到(97.38±0.28)%;能被NDV激活的CD4+T细胞表面分子CD25和CD69双阳性表达率可达(29.30±1.08)%,与PBS阴性对照组(2.40±1.30)%相比,差异有统计学意义(P<0.05);FCM检测结果显示,与对照组比较,NDV7793刺激的CD4+T细胞TRAIL表达水平均有显著升高,且在NDV7793效价为25 HU时达到最大值。结论:NDV7793可刺激CD3抗体、CD28抗体和IL-2预先活化的CD4+T细胞表达TRAIL。
Objective：To study the TRAIL up-regulation in human CD4＋T cells which stimulated by NDV7793. Method：Pure CD4＋T cells were isolated by using MACS. The CD4＋T cells were pre-activated with anti-CD3/anti-CD28 antibodies and IL-2 at first. And then after pre-activated CD4＋T cells were stimulated by NDV7793,the expression level of TRAIL was detected by FCM.Result：The purity of CD4＋T cells was（97.38±0.28）%. The CD25,CD69 cells accounted for（29.30±1.08）%after activated which was higher than that（2.40±1.30）%of the negative control group. FCM results indicated,the expression of TRAIL increased significantly when CD4＋T cells stimulated by NDV7793 compared with the control group,and reached the highest when NDV7793 at 25 HU.Conclusion：NDV7793 can up-regulate the expression of TRAIL and IFNγof pre-activated CD4＋T cells.
出处
《中国医学创新》
CAS
2014年第9期1-3,共3页
Medical Innovation of China
基金
广西自然科学基金资助项目(2013GXNSFBA019160)
广西医学科学实验中心开放基金项目(KFJJ2011-21)
