Section of Cell and Developmental Biology, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093, USA.
1] Department of Pediatrics, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093, USA. [2] Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093, USA.
Nat Rev Microbiol. 2014 Sep;12(9):624-34. doi: 10.1038/nrmicro3325.
Many bacterial and viral pathogens block or subvert host cellular processes to promote successful infection. One host protein that is targeted by invading pathogens is the small GTPase RAB11, which functions in vesicular trafficking. RAB11 functions in conjunction with a protein complex known as the exocyst to mediate terminal steps in cargo transport via the recycling endosome to cell-cell junctions, phagosomes and cellular protrusions. These processes contribute to host innate immunity by promoting epithelial and endothelial barrier integrity, sensing and immobilizing pathogens and repairing pathogen-induced cellular damage. In this Review, we discuss the various mechanisms that pathogens have evolved to disrupt or subvert RAB11-dependent pathways as part of their infection strategy.
许多细菌和病毒病原体通过阻断或颠覆宿主细胞过程来促进成功感染。一种被入侵病原体靶向的宿主蛋白是小 GTPase RAB11,它在囊泡运输中发挥作用。RAB11 与一种称为外泌体的蛋白质复合物协同作用,介导通过再循环内体到细胞-细胞连接处、吞噬体和细胞突起的货物运输的终末步骤。这些过程通过促进上皮和内皮屏障完整性、感应和固定病原体以及修复病原体诱导的细胞损伤,有助于宿主先天免疫。在这篇综述中,我们讨论了病原体进化出的各种机制,以破坏或颠覆 RAB11 依赖性途径,作为其感染策略的一部分。