Serovars of Salmonella enterica cause both gastrointestinal and systemic diseases in a broad range of mammalian hosts, including humans. Salmonella virulence depends in part on its pathogenicity island 2 type III secretion system (SPI-2 T3SS), which is required to translocate at least 28 effector proteins from vacuolar-resident bacteria into host cells. Comparative genomic analysis reveals that all serovars encode a subset of “core” effectors, suggesting that they are critical for virulence in different hosts. An additional subset of effectors is found sporadically throughout different serovars, and several inhibit activation of the innate immune system. In this Review, we summarize the biochemical activities, host cell interaction partners, and physiological functions of SPI-2 T3SS effectors in the context of the selective pressures encountered by S. enterica in vivo. We also consider some of the remaining challenges to achieve a unified understanding of how effector activities work together to promote Salmonella virulence.

肠沙门氏菌血清型在包括人类在内的广泛哺乳动物宿主中引起胃肠道和全身性疾病。沙门氏菌毒力部分取决于其致病性岛 2 III 型分泌系统 (SPI-2 T3SS)，该系统需要将至少 28 种效应蛋白从液泡驻留细菌转移到宿主细胞中。比较基因组分析表明，所有血清型都编码“核心”效应子的一个子集，这表明它们对不同宿主的毒力至关重要。在不同的血清型中偶尔发现了一个额外的效应子子集，其中一些抑制了先天免疫系统的激活。在这篇综述中，我们总结了 SPI-2 T3SS 效应器在S. enterica 体内遇到的选择压力的背景下的生化活性、宿主细胞相互作用伙伴和生理功能. 我们还考虑了一些剩余的挑战，以实现对效应活动如何协同工作以促进沙门氏菌毒力的统一理解。