RESUMEN
The review discusses information on the development of type 1 diabetes mellitus (T1D) as a systemic autoimmune and inflammatory disease. Focus of the review is on the role of innate immune system, including activation of some signaling cascades, cytokine response, and activity of the Toll-like receptors in the development of T1D. Dysfunction of innate immunity is the cause of the attack of pancreatic beta cells by the host T-lymphocytes, which leads to the death of pancreatic beta cells that produce insulin. Lack of insulin causes hyperglycemia and the need for lifelong injections of insulin in patients with T1D, which, nevertheless, does not exclude damage to many organs and tissues, given particular vulnerability of the blood vessels under conditions of hyperglycemia. The review discusses the role of oxidative stress as a factor that plays a major role in damage of vascular system and pancreatic tissue during the development of T1D. Considering high sensitivity of pancreatic beta cells to the action of reactive oxygen species (ROS), the possibility of using antioxidants for reducing the level of pathological consequences in the course of T1D development is discussed. New information on anti-diabetic activity of the exogenous antioxidant enzyme peroxiredoxin 6, which is capable of penetrating cells, activating insulin production in beta cells, reducing ROS levels, as well as decreasing activation of some signaling cascades, production of pro-inflammatory cytokines, and expression of Toll-like receptors in beta cells and in immune cells during T1D development is discussed.