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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 investigate whether NDV7793, a NDV attenuator, can promote the expression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in human CD4 + T cells. Methods: Peripheral blood CD4 + T cells were sorted by magnetic activated cell sorting (MACS), and then anti-CD3 antibody, anti-CD28 antibody and interleukin-2 (IL- 2) Make CD4 + T cells that can be activated by NDV. The expression of TRAIL in NDV-stimulated CD4 + T cells was detected by flow cytometry (FCM). Results: The purity of CD4 + T cells obtained by MACS was (97.38 ± 0.28)%, and the positive rate of CD25 and CD69 on CD + + T cells activated by NDV was (29.30 ± 1.08)%, Compared with the PBS negative control group (2.40 ± 1.30)%, the difference was statistically significant (P <0.05). The FCM results showed that compared with the control group, the TRAIL expression level of CD4 + T cells stimulated by NDV7793 increased significantly , And reached a maximum when NDV7793 titer was 25 HU. CONCLUSION: NDV7793 stimulates CD3, CD28 and IL-2 pre-activated CD4 + T cells to express TRAIL.