Multifaceted roles of RNA editing enzyme ADAR1 in innate immunity

The ADAR1–dsRNA–MDA5 axis of innate immunity. In their unedited form, long cytoplasmic dsRNAs serve as substrates for MDA5 filament formation, leading to the induction of interferon response. By catalyzing A-to-I editing in endogenous dsRNAs, ADAR1 prevents MDA5 oligomerization and constitutive interferon activation. Boxes indicate the physiological consequences of genetic perturbations of ADAR1 and MDA5 activity in mice and humans.