Abstract：
Microbial pathogens have evolved complex mechanisms to interface with host cells in order to evade host defenses and replicate. However, mammalian innate immune receptors detect the presence of molecules unique to the microbial world or sense the activity of virulence factors, activating antimicrobial and inflammatory pathways. We focus on how studies of the major virulence factor of one group of microbial pathogens, the type III secretion system (T3SS) of human pathogenic Yersinia, have shed light on these important innate immune responses. Yersinia are largely extracellular pathogens, yet they insert T3SS cargo into target host cells that modulate the activity of cytosolic innate immune receptors. This review covers both the host pathways that detect the Yersinia T3SS and the effector proteins used by Yersinia to manipulate innate immune signaling.
摘要：
微生物病原体已经进化出与宿主细胞接口的复杂机制，以逃避宿主防御和复制。然而,哺乳动物先天性免疫受体检测微生物世界特有分子的存在或感知毒力因子的活性，激活抗菌和炎症途径。我们专注于研究一组微生物病原体的主要毒力因子，人类致病性耶尔森氏菌的III型分泌系统（T3SS），揭示了这些重要的先天免疫反应。耶尔森氏菌主要是细胞外病原体，然而，他们将T3SS货物插入到调节细胞溶质先天免疫受体活性的靶宿主细胞中。这篇综述涵盖了检测耶尔森氏菌T3SS的宿主途径和耶尔森氏菌用于操纵先天免疫信号的效应蛋白。
