Kohl S, Harmon M W, Tang J P
Pediatr Res. 1983 Nov;17(11):868-72. doi: 10.1203/00006450-198311000-00006.
The ability of rotavirus-infected cells to stimulate leukocytes to release a cytokine which enhanced the subsequent leukocyte cytotoxicity to a second set of [51Cr] labeled rotavirus-infected cells was analyzed. Human interferon increased leukocyte cytotoxicity to Simian rotavirus (SA-11)-infected target cells. Similarly, 11 of 12 supernates of SA-11-stimulated peripheral blood leukocyte cultures increased the killing of SA-11-infected cells (P less than 0.005). This resulted in a calculated cytokine-dependent cellular cytotoxicity value of 9.6 +/- 1.9%. Three of five of the supernates tested contained measurable levels of interferon (12-48 unit/ml). In contrast, SA-11-stimulated colostral leukocyte culture supernates neither increased leukocyte cytotoxicity nor contained measurable levels of interferon.
分析了轮状病毒感染细胞刺激白细胞释放一种细胞因子的能力，该细胞因子可增强随后白细胞对第二组[51Cr]标记的轮状病毒感染细胞的细胞毒性。人干扰素可增强白细胞对猿猴轮状病毒（SA-11）感染的靶细胞的细胞毒性。同样，SA-11刺激的外周血白细胞培养物的12个上清液中有11个增强了对SA-11感染细胞的杀伤作用（P小于0.005）。由此计算出细胞因子依赖性细胞毒性值为9.6±1.9%。所检测的5个上清液中有3个含有可测量水平的干扰素（12 - 48单位/毫升）。相比之下，SA-11刺激的初乳白细胞培养物上清液既未增强白细胞细胞毒性，也未含有可测量水平的干扰素。
