Protein Triggers Immune Response in Lupus Patients

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.”

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