Division of Infection and Immunity, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia; email:
Annu Rev Microbiol. 2013;67:243-69. doi: 10.1146/annurev-micro-092412-155730. Epub 2013 Jun 26.
One of the most fascinating and remarkable features of Plasmodium parasites, which cause malaria, is their choice of erythrocytes as the principal host cells in which to reside during infection of a vertebrate host. Parasites completely renovate the terminally differentiated cells, which lack most of the normal organelles and functions of other cells, such as a nucleus and the machinery to express and transport proteins to subcellular locations. Erythrocyte remodeling begins immediately after invasion by the Plasmodium parasite, by expression and export of many hundreds of proteins that assemble into molecular machinery in the host cell that permit protein trafficking, harvesting of nutrients, and mechanisms to evade host immune responses. In this review, we discuss recent studies on erythrocyte remodeling, including mechanisms of protein export as well as the identity, functions, and subcellular locations of key exported proteins.
疟原虫是引起疟疾的病原体,其最显著的特征之一是选择红细胞作为其主要宿主细胞,在脊椎动物宿主感染期间寄生在红细胞内。寄生虫会彻底改造终末分化的红细胞,使其缺乏大多数正常细胞器和其他细胞的功能,如细胞核和表达和运输蛋白质到亚细胞位置的机制。红细胞重塑在疟原虫寄生虫入侵后立即开始,通过表达和输出数百种蛋白质,这些蛋白质在宿主细胞中组装成分子机制,允许蛋白质运输、营养物质的获取以及逃避宿主免疫反应的机制。在这篇综述中,我们讨论了红细胞重塑的最新研究,包括蛋白质输出的机制以及关键输出蛋白的身份、功能和亚细胞定位。