The Sainsbury Laboratory, Norwich Research Park, Norwich NR4 7UH, United Kingdom.
The Sainsbury Laboratory, Norwich Research Park, Norwich NR4 7UH, United Kingdom.
Curr Opin Microbiol. 2015 Feb;23:14-22. doi: 10.1016/j.mib.2014.10.009. Epub 2014 Nov 13.
During infection, microbes are detected by surface-localized pattern recognition receptors (PRRs), leading to an innate immune response that prevents microbial ingress. Therefore, successful pathogens must evade or inhibit PRR-triggered immunity to cause disease. In the past decade, a number of type-III secretion system effector (T3Es) proteins from plant pathogenic bacteria have been shown to suppress this layer of innate immunity. More recently, the detailed mechanisms of action have been defined for several of these effectors. Interestingly, effectors display a wide array of virulence targets, being able to prevent activation of immune receptors and to hijack immune signaling pathways. Besides being a fascinating example of pathogen-host co-evolution, effectors have also emerged as valuable tools to dissect important biological processes in host cells.
在感染过程中,微生物被表面定位的模式识别受体 (PRR) 检测到,导致先天免疫反应,从而防止微生物入侵。因此,成功的病原体必须逃避或抑制 PRR 触发的免疫反应才能引起疾病。在过去的十年中,已经证实来自植物病原菌的许多 III 型分泌系统效应蛋白 (T3E) 能够抑制这一层先天免疫。最近,已经为其中一些效应物定义了详细的作用机制。有趣的是,效应物表现出广泛的毒力靶标,能够阻止免疫受体的激活并劫持免疫信号通路。除了是病原体-宿主共同进化的一个迷人例子外,效应物也已成为剖析宿主细胞中重要生物学过程的有价值工具。