Jorgensen Ine, Rayamajhi Manira, Miao Edward A
Department of Immunology, Oslo University Hospital, Sognsvannsveien 20, Rikshospitalet 0372, Oslo, Norway.
Camargo Pharmaceutical Services, 2505 Meridian Parkway, Suite 175, Durham, North Carolina 27713, USA.
Nat Rev Immunol. 2017 Mar;17(3):151-164. doi: 10.1038/nri.2016.147. Epub 2017 Jan 31.
Eukaryotic cells can die from physical trauma, which results in necrosis. Alternatively, they can die through programmed cell death upon the stimulation of specific signalling pathways. In this Review, we discuss the role of different cell death pathways in innate immune defence against bacterial and viral infection: apoptosis, necroptosis, pyroptosis and NETosis. We describe the interactions that interweave different programmed cell death pathways, which create complex signalling networks that cross-guard each other in the evolutionary 'arms race' with pathogens. Finally, we describe how the resulting cell corpses - apoptotic bodies, pore-induced intracellular traps (PITs) and neutrophil extracellular traps (NETs) - promote the clearance of infection.
真核细胞可因物理创伤而死亡，导致坏死。或者，它们可在特定信号通路的刺激下通过程序性细胞死亡而死亡。在本综述中，我们讨论了不同细胞死亡途径在针对细菌和病毒感染的固有免疫防御中的作用：凋亡、坏死性凋亡、焦亡和中性粒细胞胞外陷阱形成。我们描述了交织不同程序性细胞死亡途径的相互作用，这些相互作用形成了复杂的信号网络，在与病原体的进化“军备竞赛”中相互交叉保护。最后，我们描述了由此产生的细胞尸体——凋亡小体、孔诱导的细胞内陷阱（PITs）和中性粒细胞胞外陷阱（NETs）——如何促进感染的清除。
