West A Phillip
Department of Microbial Pathogenesis and Immunology, Texas A&M University Health Science Center, 470 Reynolds Medical Building, TAMU 1114, College Station, TX 77843, USA.
Toxicology. 2017 Nov 1;391:54-63. doi: 10.1016/j.tox.2017.07.016. Epub 2017 Jul 29.
A growing literature indicates that mitochondria are key participants in innate immune pathways, functioning as both signaling platforms and contributing to effector responses. In addition to regulating antiviral signaling and antibacterial immunity, mitochondria are also important drivers of inflammation caused by sterile injury. Much research on mitochondrial control of immunity now centers on understanding how mitochondrial constituents released during cellular damage simulate the innate immune system. When mitochondrial integrity is compromised, mitochondrial damage-associated molecular patterns engage pattern recognition receptors, trigger inflammation, and promote pathology in an expanding list of diseases. Here, I review the emerging knowledge of mitochondrial dysfunction in innate immune responses and discuss how environmental exposures may induce mitochondrial damage to potentiate inflammation and human disease.
越来越多的文献表明，线粒体是先天免疫途径的关键参与者，既是信号平台，又有助于效应反应。除了调节抗病毒信号和抗菌免疫外，线粒体也是无菌损伤引起的炎症的重要驱动因素。目前，关于线粒体对免疫的控制的许多研究都集中在了解细胞损伤期间释放的线粒体成分如何模拟先天免疫系统。当线粒体完整性受到损害时，线粒体损伤相关分子模式会与模式识别受体结合，触发炎症，并在越来越多的疾病中促进病理过程。在这里，我回顾了先天免疫反应中线粒体功能障碍的新知识，并讨论了环境暴露如何诱导线粒体损伤以增强炎症和人类疾病。
