Mitochondrial ROS signals prevent excessive immune response

Reactive oxygen species (ROS) were long considered unwanted and dangerous by-products of mitochondrial metabolism, specifically oxidative phosphorylation. More recently, evidence has indicated that mitochondrial ROS are also essential signalling molecules that unexpectedly promote longevity, through a mechanism termed mitohormesis. In this issue, Timblin et al. expand this concept to immunity, specifically macrophage function, by demonstrating that mitochondrial ROS are required to prevent an excessive immune response.