Kitaguchi T, Nagoya M, Amano T, Suzuki M, Minami M
Department of Parasitology, School of Medicine, Yokohama City University, Japan.
Parasitol Res. 1996;82(4):352-7. doi: 10.1007/s004360050125.
Mice that have recovered from a primary infection with Plasmodium chabaudi have been shown to resist a secondary infection. In the present study the authors investigated how natural killer (NK) cells were involved in this resistance. Spleen cells from P. chabaudiprimed C57BL/6 mice could transfer protection against P. chabaudi infection into naive syngeneic mice, but spleen cells from unprimed mice could not. T-enriched cells purified from primed spleen cells could also transfer such protection. Transfer of NK cells from primed spleen cells failed to protect against challenge infection. However, depletion of NK cells in host mice by injection of an anti-NK1.1 monoclonal antibody resulted in higher mortality relative to controls. The possible protective roles of NK cells in P. chabaudi infection are discussed.
已证明从查巴迪疟原虫初次感染中恢复的小鼠能够抵抗二次感染。在本研究中，作者调查了自然杀伤（NK）细胞是如何参与这种抵抗力的。来自经查巴迪疟原虫致敏的C57BL/6小鼠的脾细胞可以将针对查巴迪疟原虫感染的保护作用转移到同基因的未致敏小鼠中，但来自未致敏小鼠的脾细胞则不能。从致敏脾细胞中纯化的富含T细胞也可以转移这种保护作用。从致敏脾细胞转移NK细胞未能预防攻击感染。然而，通过注射抗NK1.1单克隆抗体使宿主小鼠中的NK细胞耗竭，导致相对于对照组更高的死亡率。讨论了NK细胞在查巴迪疟原虫感染中可能的保护作用。
