Abstract
Type 1 diabetes mellitus is an autoimmune disease of pancreatic beta cells. The morfological and functional abnormalities of immune cells are detectable in the islets of Langerhans and partly in the peripheral blood at the time of disease onset.
The crucial role in the pathogenesis of the disease plays Th-1 subpopulation of CD 4+ cells which coordinates immune response and induces and accelerates destruction of pancreatic beta cells through interleukin 2 and interferon gamma. Th-2 subpopulation competes with Th-1 subpopulation and plays protective role in the pathogenesis of type 1 diabetes mellitus.
Type 1 diabetes mellitus originates in the disbalance of the both subpopulations. The transplantation of Th-1 cells transmits diabetes.
CD 8+ cells destruct directly pancreatic beta cells by the cytotoxic mediators. NK cells product interleukin 4 and interleukin 10.
Both IL-4 and IL-10 shift immune response in favour of Th-2 pathway. The morfological and functional defects of NK cells are detectable.
B lymphocytes cooperate with the other immune cells and product antibodies - the main marker of insulitis in the peripheral blood.