van der Heyde H C, Pepper B, Batchelder J, Cigel F, Weidanz W P
Department of Medical Microbiology and Immunology, University of Wisconsin, Madison 53706, USA.
Exp Parasitol. 1997 Feb;85(2):206-13. doi: 10.1006/expr.1996.4132.
Murine malarial parasites have long been characterized by their requirement for either antibody-mediated immunity (AMI) or cell-mediated immunity (CMI) for suppression of acute parasitemia, with Plasmodium yoelii reportedly requiring AMI for suppression and P. chabaudi requiring CMI. To assess this characterization in terms of the current T(H1)/T(H2)-CMI/AMI hypothesis, we infected gene-targeted "knockout" mice lacking either a type-1 cytokine (IL-2 or IFN-gamma) or a type-2 cytokine (IL-4 or IL-10) with one or the other species of Plasmodium. We observed that type-1 cytokine-deficient mice developed exacerbated malaria with either P. yoelii or P. chabaudi, compared with that seen in heterozygote controls. Moreover, type-2 cytokine knockout mice showed a similar time course of infection with either parasite compared with that seen with their controls. We conclude that the mechanism of resolution of these well characterized malarial infections cannot be linked definitely to these T(H1)- and T(H2)-associated cytokines as predicted by the T(H1)/T(H2)-CMI/AMI hypothesis.
长期以来，鼠疟原虫的特征在于，其急性寄生虫血症的抑制需要抗体介导的免疫（AMI）或细胞介导的免疫（CMI），据报道，约氏疟原虫的抑制需要AMI，而查巴迪疟原虫的抑制需要CMI。为了根据当前的T(H1)/T(H2)-CMI/AMI假说评估这一特征，我们用其中一种疟原虫感染了缺乏1型细胞因子（IL-2或IFN-γ）或2型细胞因子（IL-4或IL-10）的基因靶向“敲除”小鼠。我们观察到，与杂合子对照相比，缺乏1型细胞因子的小鼠感染约氏疟原虫或查巴迪疟原虫后疟疾病情加重。此外，缺乏2型细胞因子的敲除小鼠感染这两种寄生虫中的任何一种后的感染时间进程与对照相似。我们得出结论，这些特征明确的疟疾感染的消退机制不能像T(H1)/T(H2)-CMI/AMI假说所预测的那样，肯定地与这些T(H1)和T(H2)相关细胞因子联系起来。
