Liu Jing-Mei, Zhu Yong, Xu Zhu-Wei, Ouyang Wei-Ming, Wang Jiu-Ping, Liu Xue-Song, Cao Yun-Xin, Li Qi, Fang Liang, Zhuang Ran, Yang An-Gang, Jin Bo-Quan
Department of Immunology, Fourth Military Medical University, Xi'an, China.
Clin Immunol. 2006 Jun;119(3):245-51. doi: 10.1016/j.clim.2006.02.010. Epub 2006 Apr 17.
The expression of the apoptosis-inducing ligands, TNF-alpha, FasL and TRAIL on peripheral blood mononuclear cells (PBMC) and the levels of their soluble form (TNF-alpha, sFasL and sTRAIL) in plasma from 40 hemorrhagic fever with renal syndrome (HFRS) patients as well as 26 healthy blood donors were determined by flow cytometry (FCM) analysis and sandwich ELISA, respectively. The status of Th1, Th2, Tc1 and Tc2 subsets in PBMC was evaluated by intracellular cytokine staining and FCM. Compared to controls, the expression of membrane bound FasL and TRAIL was up-regulated on surface of PBMC isolated from the HFRS patients, particularly on CD8+ T lymphocytes. The levels of TNF-alpha, sFasL and sTRAIL in plasma from the HFRS patients in the acute phase increase 4.7-fold, 6.0-fold and 1.8-fold, respectively, over those from the healthy donors. The percentage of Th1, Tc1 and Tc2 subsets in PBMC from the patients also increased significantly compared with those from healthy donors. These results indicate that dynamic changes occurred in both the membrane bound and soluble forms of apoptosis-inducing ligands (FasL, TRAIL and TNF-alpha) and proportions of Th1 and CTL in HFRS patients increased. Both factors may play an important role in the etiology of Hantaan virus infection in humans.
分别采用流式细胞术（FCM）分析和夹心酶联免疫吸附测定法，检测了40例肾综合征出血热（HFRS）患者外周血单个核细胞（PBMC）上凋亡诱导配体TNF-α、FasL和TRAIL的表达及其血浆中可溶性形式（TNF-α、sFasL和sTRAIL）的水平，同时检测了26名健康献血者的上述指标。通过细胞内细胞因子染色和FCM评估PBMC中Th1、Th2、Tc1和Tc2亚群的状态。与对照组相比，HFRS患者分离的PBMC表面膜结合FasL和TRAIL的表达上调，尤其是在CD8+T淋巴细胞上。急性期HFRS患者血浆中TNF-α、sFasL和sTRAIL的水平分别比健康献血者高出4.7倍、6.0倍和1.8倍。与健康献血者相比，患者PBMC中Th1、Tc1和Tc2亚群的百分比也显著增加。这些结果表明，HFRS患者凋亡诱导配体（FasL、TRAIL和TNF-α）的膜结合形式和可溶性形式均发生动态变化，且Th1和CTL的比例增加。这两个因素可能在汉坦病毒感染人类的病因学中起重要作用。
