Immunohistochemical study of the pancreas of patients with long termed diabetes mellitus type 1

Abstract

There has been a concept of the autoimmune pathogenesis of DM1 developed in the diabetology. The basic notion of the concept is that a root cause of a death of the insulin containing B-cells is in an autoimmune aggression against them (1, 2). There is a significant destruction of B-cells observed in patients with DM1 prior to diagnosis. In patients with recently diagnosed DM1 the autoimmune processes has manifested in a form of insulitis chronic inflammatory infiltration of mononuclear cells in the residual cells of the pancreatic islets (3). Although considered typical for recent onset disease, the insulitis has been described only in approximately 150 cases per 100 years (4). It is known that DM1 is accompaniedby peripheral nervous system lesions wich leads to a reduction of a life span and mortality enlargement. It has been suggested that peripheral nervous system lesions, as well as B-cell destruction, in DM1 patients also has an autoimmune nature. Moreover, experiments on DM1 animal models (NOD mice) shows the autoimmune destruction of pancreatic nerve terminals at a beginning of the DM1 progression (5-11). According to this model the autoimmune reaction on B-cells develops after T-cells infiltration into the pancreatic islets as a result of similarities between B-cells and neurons in some synthezied proteins and intracellular processes, and high sensitivity of B-cells to the cytokine induced destruction (5, 6, 12,13).