CAJ | 학술논문

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。
목적：연구신성역병독（Newcastle disease virus，NDV）약독주NDV7793능부촉진인CD4+T세포표체종류배사인자상관조망인자유도배체（TNF-related apoptosis-inducing ligand，TRAIL）。방법：수선용면역자주분선법（magnetic activated cell sorting，MACS）분선외주혈정지CD4+T세포，연후가항CD3항체、항CD28항체화백세포개소-2（interleukin-2，IL-2）사지성위능피NDV격활적CD4+T세포。용류식세포기술（flow cytometry， FCM）검측NDV자격적CD4+T세포적TRAIL적표체수평。결과：MACS법분선외주혈득도적CD4+T세포순도체도（97.38±0.28）%；능피NDV격활적CD4+T세포표면분자CD25화CD69쌍양성표체솔가체（29.30±1.08）%，여PBS음성대조조（2.40±1.30）%상비，차이유통계학의의（P<0.05）；FCM검측결과현시，여대조조비교， NDV7793자격적CD4+T세포TRAIL표체수평균유현저승고，차재NDV7793효개위25 HU시체도최대치。결론：NDV7793가자격CD3항체、CD28항체화IL-2예선활화적CD4+T세포표체TRAIL。
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.