Mitochondria in innate immune responses
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TL;DR: This work reviews the emerging knowledge about the roles of mitochondria in innate immunity and suggests mitochondria appear to function as centrally positioned hubs in the innate immune system.
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Abstract: The innate immune system has a key role in the mammalian immune response. Recent research has demonstrated that mitochondria participate in a broad range of innate immune pathways, functioning as signalling platforms and contributing to effector responses. In addition to regulating antiviral signalling, mounting evidence suggests that mitochondria facilitate antibacterial immunity by generating reactive oxygen species and contribute to innate immune activation following cellular damage and stress. Therefore, in addition to their well-appreciated roles in cellular metabolism and programmed cell death, mitochondria appear to function as centrally positioned hubs in the innate immune system. Here, we review the emerging knowledge about the roles of mitochondria in innate immunity.
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TL;DR: It is shown that mitophagy/autophagy blockade leads to the accumulation of damaged, ROS-generating mitochondria, and this in turn activates the NLRP3 inflammasome, and may explain the frequent association of mitochondrial damage with inflammatory diseases.
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Circulating mitochondrial DAMPs cause inflammatory responses to injury
Qin Zhang,Mustafa Raoof,Yu Chen,Yuka Sumi,Tolga Sursal,Wolfgang G. Junger,Karim Brohi,Kiyoshi Itagaki,Carl J. Hauser +8 more
TL;DR: It is shown that injury releases mitochondrial DAMPs into the circulation with functionally important immune consequences, including formyl peptides and mitochondrial DNA, which promote PMN Ca2+ flux and phosphorylation of mitogen-activated protein (MAP) kinases, thus leading to PMN migration and degranulation in vitro and in vivo.
Identification and Characterization of MAVS, a Mitochondrial Antiviral Signaling Protein that Activates NF-κB and IRF3
TL;DR: The identification of a novel protein termed MAVS (mitochondrial antiviral signaling), which mediates the activation of NF-kappaB and IRF 3 in response to viral infection, and implicates a new role of mitochondria in innate immunity.
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