登革病毒诱导的细胞毒素由脾细胞释放亚硝酸盐。
Dengue virus-induced cytotoxin releases nitrite by spleen cells.
作者信息
Mukerjee R, Misra A, Chaturvedi U C
机构信息
Department of Microbiology, K.G. Medical College, Lucknow, India.
出版信息
Int J Exp Pathol. 1996 Apr;77(2):45-51. doi: 10.1046/j.1365-2613.1996.962100.x.
Dengue type-2 virus (DV) infection in mice induces T cells to produce a cytokine, the cytotoxic factor (CF), which induces H2-A positive macrophages to produce another cytokine, cyototoxic (CF2), which amplifies its cytotoxic effects on target cells. The present study was undertaken to investigate the production of nitrite (NO2-) by the spleen cells of mice in vitro and in vivo following inoculation of CF2. Maximum NO2- production occurred at 1 hour after inoculation of 100 micrograms CF2. Pretreatment of CF2 with anti-CF2-antisera (CF2-As) inhibited the production of NO2-. Pretreatment of the spleen cells with NG-monomethyl-L-arginine (NMA) or with arginase inhibited NO2- production. The NO2- production was diminished in a dose dependent manner by treatment of spleen cells with the Ca2+ channel blocking drug, nifedipine and Zn2+ as ZnSO4. The findings of the present study thus demonstrate that CF2 induces production of NO2- in the spleen cells in a CA(2+)-dependent manner which may be a mechanism of target cell killing.
2型登革病毒（DV）感染小鼠会诱导T细胞产生一种细胞因子，即细胞毒性因子（CF），该因子会诱导H2-A阳性巨噬细胞产生另一种细胞因子，即细胞毒性因子2（CF2），后者会增强其对靶细胞的细胞毒性作用。本研究旨在调查接种CF2后，小鼠脾细胞在体外和体内产生亚硝酸盐（NO2-）的情况。接种100微克CF2后1小时，NO2-产生量达到最大值。用抗CF2抗血清（CF2-As）预处理CF2可抑制NO2-的产生。用NG-单甲基-L-精氨酸（NMA）或精氨酸酶预处理脾细胞可抑制NO2-的产生。用钙通道阻滞剂硝苯地平和硫酸锌形式的锌离子处理脾细胞，NO2-的产生会以剂量依赖的方式减少。因此，本研究结果表明，CF2以钙依赖的方式诱导脾细胞产生NO2-，这可能是靶细胞杀伤的一种机制。
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