Scientists have discovered that reactive oxygen species (ROS) produced by mitochondria trigger the clustering of MAVS driving IFN production. When ROS were inhibited, scientists were able to prevent MAVS oligomerization — or the joining together of several MAVS molecules — and, consequently, to avoid type I IFN production.
The results suggest that mitochondria oxidative stress, or ROS buildup inside cells, promotes a type I IFN response in lupus patients. The findings also suggest that targeting MAVS is a potential therapeutic strategy directed towards mitochondria that could prove beneficial for SLE patients.
“We need to develop a drug that can revive the mitochondria,” Buskiewicz said. “A more focused antioxidant therapy targeting the particular organelle may have more efficacy.”