Niederkorn J Y, Brieland J K, Mayhew E
Infect Immun. 1983 Jul;41(1):302-7. doi: 10.1128/iai.41.1.302-307.1983.
Spleen cells from mice infected with the protozoan parasite Encephalitozoon cuniculi demonstrated enhanced in vitro cytolysis of YAC-1 lymphoma cells. Selective cell depletion experiments showed that the dominant cell population mediating cytolysis of YAC-1 tumor cells expressed the characteristic phenotype of murine natural killer (NK) cells because (i) pretreatment of spleen cells with anti-asialo GM 1 antiserum plus complement abolished the cytotoxic activity; (ii) augmented cytolysis was found in athymic nude mice; (iii) pretreatment of spleen cells with anti-Thy 1.2 plus complement did not affect the level of cytolysis; and (iv) nylon wool removal of adherent cells did not reduce the augmented cytolysis. The augmented cytolysis peaked 7 days after infection, gradually diminished, and finally returned to control levels by 21 days postinfection. The parasite-induced augmentation of NK cell activity was dose-dependent: inoculation of 10(7) parasites gave maximum enhancement, whereas 10(5) or 10(4) parasites had an insignificant effect on spontaneous NK cell cytolysis. The augmented NK cell cytotoxicity was dependent upon viable parasites; inoculation of killed parasites failed to stimulate a significant increase in spontaneous cytolysis. An active infectious process was an important component of this process. The peak of NK activity in euthymic mice was closely correlated with the active stage of infection, and reduction of NK cell activity coincided with recovery from infection. By contrast, athymic nude mice were unable to control E. cuniculi infections yet maintained persistently elevated NK responses. The present data, along with previous reports, indicate that infection with E. cuniculi evokes transient modulation of host immune functions.
感染原生动物寄生虫兔脑炎微孢子虫的小鼠脾细胞，在体外对YAC-1淋巴瘤细胞的细胞溶解作用增强。选择性细胞清除实验表明，介导YAC-1肿瘤细胞溶解的主要细胞群体表达了小鼠自然杀伤（NK）细胞的特征性表型，因为：（i）用抗唾液酸GM1抗血清加补体预处理脾细胞可消除细胞毒性活性；（ii）在无胸腺裸鼠中发现细胞溶解作用增强；（iii）用抗Thy 1.2加补体预处理脾细胞不影响细胞溶解水平；（iv）用尼龙毛去除贴壁细胞不降低增强的细胞溶解作用。增强的细胞溶解作用在感染后7天达到峰值，随后逐渐减弱，最终在感染后21天恢复到对照水平。寄生虫诱导的NK细胞活性增强呈剂量依赖性：接种10^7个寄生虫可产生最大增强作用，而接种10^5或10^4个寄生虫对自发NK细胞溶解作用影响不显著。增强的NK细胞细胞毒性依赖于活的寄生虫；接种灭活的寄生虫未能刺激自发细胞溶解作用显著增加。活跃的感染过程是这一过程的重要组成部分。正常小鼠中NK活性的峰值与感染的活跃阶段密切相关，NK细胞活性的降低与感染的恢复同时发生。相比之下，无胸腺裸鼠无法控制兔脑炎微孢子虫感染，但NK反应持续升高。目前的数据以及先前的报道表明，兔脑炎微孢子虫感染可引起宿主免疫功能的短暂调节。
