Type III secretion systems (T3SS) play a crucial role for virulence in many Gram-negative bacteria. After tight bacterial contact to host cells, the T3SS injects effector proteins into the host cells, which leads to cell invasion, tissue destruction and/or immune evasion. Over the last decade several attempts were made to characterize the host-cell interactions which precede and determine effector protein injection during infection. The development of the TEM-β-lactamase reporter was an important breakthrough to achieve this goal. By this means it was demonstrated that during infection with many Gram-negative pathogens such as Salmonella, Pseudomonas or Yersinia the main targets of T3SS are leukocytes of the myeloid lineage such as neutrophils, macrophages or dendritic cells. This is due to the recruitment of these cells to the site of infection, but also due to the specific interplay between bacterial and host cells. Comprehensive studies on Yersinia pestis, Yersinia enterocolitica and Yersinia pseudotuberculosis effector translocation show that adhesins such as Invasin (Inv), Yersinia adhesin A (YadA) and attachment and invasion locus (Ail) are critical for effector translocation. Here, mainly the complex interaction of YadA and Ail with various host cell receptor repertoires on leukocytes and the modulatory effects of serum factors direct effector translocation predominantly towards myeloid cells. The current understanding suggests that mostly protein based interactions between bacteria and host determine host cell specific effector translocation during Yersinia infection. However, for Shigella dysenteriae infection it was shown that glycan-glycan interactions can also play a critical role for the adhesion preceding effector translocation. In addition, the Shigella infection model revealed that the activation status of cells is a further criterium directing effector translocation into a distinct cell population. In this review the current understanding of the complex and species-specific interaction between bacteria and host cells leading to type III secretion is discussed.

III型分泌系统（T3SS）对许多革兰氏阴性细菌的致病性起着至关重要的作用。在细菌与宿主细胞紧密接触后，T3SS将效应蛋白注入宿主细胞，从而导致细胞入侵，组织破坏和/或免疫逃逸。在过去的十年中，人们进行了几次尝试来表征宿主细胞之间的相互作用，该相互作用在感染前先确定感染蛋白的能力。TEM-β-内酰胺酶报告基因的开发是实现该目标的重要突破。通过这种方法表明，在感染许多革兰氏阴性病原体（如沙门氏菌，假单胞菌或耶尔森氏菌）期间T3SS的主要靶标是髓系谱系的白细胞，例如嗜中性粒细胞，巨噬细胞或树突状细胞。这是由于这些细胞募集到感染部位，也归因于细菌和宿主细胞之间的特异性相互作用。对鼠疫耶尔森氏菌，小肠结肠炎耶尔森氏菌和假结核耶尔森氏菌效应子易位的综合研究表明，粘附素如Invasin（Inv），耶尔森氏菌粘附素A（YadA）以及附着和侵袭位点（Ail）对于效应子易位至关重要。在这里，主要是YadA和Ail与白细胞上各种宿主细胞受体库的复杂相互作用以及血清因子的调节作用直接将效应子易位定向到髓样细胞。当前的理解表明，细菌和宿主之间主要基于蛋白质的相互作用决定了耶尔森氏菌感染期间宿主细胞特异性效应子的移位。然而，对于痢疾志贺氏菌感染，显示聚糖-聚糖相互作用也可在效应子易位之前的粘附中起关键作用。此外，志贺氏菌感染模型显示，细胞的激活状态是进一步的标准，将效应子转位到不同的细胞群中。在这篇综述中，讨论了导致细菌和III型分泌的细菌与宿主细胞之间复杂且物种特异性相互作用的当前理解。