Abstract
Proposed mechanisms by which disruption of endogenous dsRNA editing in β-cells leads to type 1 diabetes-like phenotypes in βAdarKO mice. Disruption of endogenous dsRNA editing in β-cells initiates IFN responses, thereby inducing pancreatic islet inflammation and β-cell dysfunction. Hyperglycemia induced by β-cell dysfunction further promotes islet inflammation, likely via increased dsRNA resulting from increased β-cell workload, thereby producing a vicious cycle. The mechanism by which impairment of dsRNA editing is integrated with autoimmune-mediated pathogenesis of type 1 diabetes remains to be clarified.