Questions about NOD mouse diabetes.

a still unknown triggering event such as the local inflammation brought by a putative virus or an antigen mimicry phenomenon. Alternatively hut not exclusively, it might involve a defect in protective immunoregulatory circuits. An intriguing possibility is that the onset of diabetes is secondary to the loss of the active tolerance that characterizes the 2-3-month-long period of clinically latent insulitis (prediabetic stage). If this is indeed the case, how does this tolerance operate (Thl/Th2 imbalance) ? What are the factors that control this loss of active tolerance ?