Albright J W, Huang K Y, Albright J F
Infect Immun. 1983 Jun;40(3):869-75. doi: 10.1128/iai.40.3.869-875.1983.
Trypanosoma musculi infection affected natural killer (NK) activity in mice. In the spleen, an increase of two to three times normal was displayed on days 2 to 4 after inoculation of parasites, followed by rapid decline to a subnormal level of activity that persisted for more than 3 weeks and included the phase of rapid parasite elimination. NK activity increased dramatically in peritoneal exudate and marrow early in infection, but the subsequent decline was more moderate than in the spleen. The subnormal splenic activity was not elevated by treating infected mice with an interferon inducer, polyinosinic acid-polycytidylic acid. Serum interferon levels were elevated early in infection, but by day 4 postinoculation, they had returned to undetectable. Injection of mice with antiserum to murine interferon-beta did not inhibit the early rise in NK activity or alter the course of trypanosome infection; in fact, the antiserum treatment enhanced splenic NK activity in infected mice. The early rise and subsequent decline of NK activity did not correlate with the course of T. musculi infection and subsequent cure. The cause of the dramatic decline in splenic NK activity is under investigation; it could result, for example, from arousal of suppressor cells, inhibition by prostaglandins, or inhibition by trypanosome-derived substances. Thus, NK cells may be prevented from fulfilling their potential of attacking the extracellular trypanosomes by the effects of inhibitory substances.
鼠锥虫感染影响小鼠的自然杀伤(NK)活性。在脾脏中,接种寄生虫后第2至4天,NK活性增加至正常水平的两到三倍,随后迅速下降至低于正常水平,并持续超过3周,这一阶段包括寄生虫快速清除阶段。感染早期,腹膜渗出液和骨髓中的NK活性显著增加,但随后的下降比脾脏中的更为缓和。用干扰素诱导剂聚肌苷酸-聚胞苷酸治疗感染小鼠,并未提高脾脏中低于正常水平的活性。感染早期血清干扰素水平升高,但接种后第4天,其水平已降至无法检测到。给小鼠注射抗小鼠干扰素-β抗血清,并未抑制NK活性的早期升高,也未改变锥虫感染的进程;事实上,抗血清治疗增强了感染小鼠脾脏中的NK活性。NK活性的早期升高和随后的下降与鼠锥虫感染及随后的治愈过程无关。脾脏NK活性急剧下降的原因正在研究中;例如,它可能是由抑制性细胞的激活、前列腺素的抑制作用或锥虫衍生物质的抑制作用导致的。因此,抑制性物质的作用可能会阻止NK细胞发挥攻击细胞外锥虫的潜能。