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. 2018 Jul 30;128(9):3651–3661. doi: 10.1172/JCI120845

Figure 2. Mitochondria-linked activation of immune pathways.

Figure 2

Mitochondrial content and structure can play integral roles in the activation of inflammatory signaling in response to stress effects or viral infections. Extracellular mtDNA can activate NF-κB–driven inflammation via the intracellular TLR9 receptor. Alternatively, released mtDNA can initiate type I IFN signaling in adjacent immune cells. In response to mitochondrial stressors, ROS-damaged mtDNA, mitochondrial ROS, and the release of cardiolipin (CL) from the IMM can activate the NLRP3 inflammasome to promote IL-1β and IL-18 signaling. The loss of mitochondrial integrity with the extrusion of mtDNA can also activate the cGAS/STING pathway and type I IFN signaling. Finally, the mitochondrion functions as a platform for the dimerization of MAVS to activate a combination of NF-κB and IFN regulator signaling in response to viral infections.