While many candidate type 1 diabetes (T1D) susceptibility genes have been identified, evidence suggests that environmental stimuli, such as viral infections, may also be involved in T1D pathogenesis. However, how viral infections may prevent or trigger the diabetogenic process remains unclear. In this issue of the JCI, Filippi et al. show that infection of NOD mice with Coxsackie virus B3 or lymphocytic choriomeningitis virus, neither of which directly destroys insulin-secreting pancreatic β cells, triggers the activation of two distinct immunoregulatory mechanisms, involving both the innate and adaptive immune system, that protect against the development of T1D in these animals (see the related article beginning on page 1515).
