An Immunologic Approach to the Pathogenesis of Type 1 Diabetes"

Abstract

 Type 1 diabetes is a T cell-mediated autoimmune disease. Genetic and environmental factors induce chronic autoimmunity against pancreatic beta cells. As time passes, autoimmunity gives rise to beta cell loss and overt diabetes. The immune system reacts against foreign substances such as microbes, and macromolecules like proteins and polysaccharides. The specific immune response is able to distinguish the body’s own macromolecules from those that are extraneous. Tolerance is a process where the immune system learns to live with macromolecules of the body in which it belongs, and maintains and develops the ability to react against foreign molecules. However, if the immune system reacts against its own members, the tolerance can be broken naturally. This can happen through cessation of the repression that prevents immune cells reacting against components of the body or by alterations in cells that the body does not recognize as self. This phenomenon is called autoimmunity. The pathogenesis begins with the activation of potentially self-reactive T lymphocytes. The serious loss of pancreatic beta cells and infiltration of pancreatic islets by lymphocytes that create insulitis represent the pathology of type 1 diabetes