先天免疫系统
炎症
线粒体
生物
模式识别受体
免疫学
免疫
效应器
免疫系统
细胞生物学
出处
期刊:Toxicology
[Elsevier]
日期:2017-07-29
卷期号:391: 54-63
被引量:198
标识
DOI:10.1016/j.tox.2017.07.016
摘要
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.
科研通智能强力驱动
Strongly Powered by AbleSci AI