Figure 3.

Diabetes type 1 viewed as a neural disorder. In this pathophysiological scheme, pathological autoimmunity against GAD65, the main targeted autoantigen in diabetes type 1, would result from both immune and neural alterations occurring concurrently. An immune stress such as, for instance, a viral infection would lead to a drop of Tregs. In parallel, a cognitive or behavioral stress (for instance cognitive overstimulation or mood imbalance) would be responsible for an increased exposure of the immune system to the brain superautoantigen GAD65. Pathological autoimmunity against pancreatic islet cells expressing GAD65 antigen would then result from an increased number, increased activation state and altered homing of GAD65 autoreactive T-cells.