School of Medicine, Deakin University, Waurn Ponds, Victoria 3216, Australia.
Department of Biochemistry and Molecular Biology, Bio21 Institute, The University of Melbourne, Victoria 3010, Australia.
Nat Rev Microbiol. 2016 Aug;14(8):494-507. doi: 10.1038/nrmicro.2016.79. Epub 2016 Jul 4.
Plasmodium parasites, the causative agents of malaria, have developed elaborate strategies that they use to survive and thrive within different intracellular environments. During the blood stage of infection, the parasite is a master renovator of its erythrocyte host cell, and the changes in cell morphology and function that are induced by the parasite promote survival and contribute to the pathogenesis of severe malaria. In this Review, we discuss how Plasmodium parasites use the protein trafficking motif Plasmodium export element (PEXEL), protease-mediated polypeptide processing, a novel translocon termed the Plasmodium translocon of exported proteins (PTEX) and exomembranous structures to export hundreds of proteins to discrete subcellular locations in the host erythrocytes, which enables the parasite to gain access to vital nutrients and to evade the immune defence mechanisms of the host.
疟原虫寄生虫是疟疾的病原体，它们已经发展出了精细的策略，用于在不同的细胞内环境中生存和繁殖。在感染的血液阶段，寄生虫是其红细胞宿主细胞的大师级改造者，寄生虫诱导的细胞形态和功能变化促进了生存，并导致严重疟疾的发病机制。在这篇综述中，我们讨论了疟原虫寄生虫如何利用蛋白运输基序疟原虫输出元件（PEXEL）、蛋白酶介导的多肽加工、一种称为疟原虫输出蛋白的转运体（PTEX）和外膜结构，将数百种蛋白输出到宿主红细胞中的离散亚细胞位置，这使寄生虫能够获得重要的营养物质，并逃避宿主的免疫防御机制。
