[Physiopathological progress in type 1 diabetes]

Type 1 diabetes results from the autoimmune destruction of pancreatic islet B cells, leading within various times to absolute insulin deficiency. The pathophysiology of the disease remains partly unclear: only half of the genetic predisposition is known; the nature, and even the reality, of a triggering event in the autoimmune activation are not established; furthermore, the primitive target of the autoimmune process is not fully determined. As immunological markers of the disease have been developped, therapeutic perspectives for type 1 diabetes prevention have emerged. However, little have been sucessful until now, reflecting the disease heterogeneity and complexity and the difficulty to define the best therapeutic window.