van der Heyde H C, Manning D D, Roopenian D C, Weidanz W P
Department of Medical Microbiology and Immunology, University of Wisconsin, Madison 53706.
J Immunol. 1993 Sep 15;151(6):3187-91.
We utilized a definitive model of CD8+ T cell deficiency, the beta 2-microglobulin-deficient (beta 2-m0/0) mouse, to determine whether CD8+ T cells are required in the resolution of blood-stage malaria. In a parallel experiment, C57Bl/6 mice treated with anti-CD8 mAb showed significantly higher levels of parasitemia than untreated C57Bl/6 control mice at several points during the infection. This finding suggests some role for CD8+ cells in containing malaria. However, the beta 2-m0/0 mice, which are genetically blocked from expressing MHC class I or class Ib glycoproteins and therefore have < 2.5% of the normal number of CD8+ T cells, nevertheless resolved infections with three virulence variants of murine Plasmodium. The resolution of Plasmodium chabaudi adami, Plasmodium yoelii yoelii 17X, and Plasmodium chabaudi chabaudi AS infections by beta 2-m0/0 mice in the virtual absence of CD8+ cells demonstrates that these cells are not required to suppress murine malaria and that the suppression mechanism is not MHC class I restricted. The similarity of the time-course for resolution of infection in beta 2-m0/0 and intact control mice with all three subspecies of Plasmodium further supports the lack of a requirement for CD8+ T cells in the suppression of malarial parasitemia.
我们利用一种明确的CD8 + T细胞缺陷模型，即β2-微球蛋白缺陷（β2-m0/0）小鼠，来确定在血液期疟疾的消退过程中是否需要CD8 + T细胞。在一项平行实验中，在感染期间的几个时间点，用抗CD8单克隆抗体处理的C57Bl/6小鼠的寄生虫血症水平明显高于未处理的C57Bl/6对照小鼠。这一发现表明CD8 +细胞在控制疟疾方面发挥了一定作用。然而，β2-m0/0小鼠由于基因缺陷无法表达MHC I类或Ib类糖蛋白，因此其CD8 + T细胞数量不到正常数量的2.5%，但它们仍然能够清除三种毒力变异的鼠疟原虫感染。β2-m0/0小鼠在几乎没有CD8 +细胞的情况下清除了恰氏疟原虫、约氏疟原虫17X株和约氏疟原虫沙巴迪株的感染，这表明这些细胞并非抑制鼠疟所必需，且抑制机制不受MHC I类限制。β2-m0/0小鼠和完整对照小鼠在感染所有三种疟原虫亚种时感染消退的时间进程相似，这进一步支持了抑制疟原虫血症不需要CD8 + T细胞这一观点。
