**2. Modern ideas about the immunopathogenesis of type 1 diabetes mellitus**

Type 1 diabetes mellitus (T1DM) is an organ-specific autoimmune disease that develops as a result of the selective destruction of b-cells of the pancreatic islet apparatus by cytotoxic T lymphocytes (CTL), T helper type 1 (Th1) and autoantibodies [1, 2]. Together with interleukin 1b (IL-1b) and tumor necrosis factor α (TNF-α), interferong (IFN-g) is able to increase the expression of molecules of the major histocompatibility complex of the second class on pancreatic b-cells. This leads to recognizing them as alien [3, 4]. As a result of the gradual destruction of b-cells, insulin deficiency occurs, leading to a breakdown in glucose homeostasis and the manifestation T1DM. Clinically classic symptoms of T1DM—hyperglycemia and ketosis, appear only when 80–90% of the islets of Langerhans are destroyed [5].

Despite the active study of the immunopathogenesis of T1DM, many key points in the development and progression of this disease remain unclear. The problems of early diagnosis of T1DM, ensuring a stable course of the disease and combating its secondary complications are still relevant [6]. Тhe manifestation of T1DM is preceded by a long asymptomatic period—the prediabetic stage. It should be emphasized that during the asymptomatic stage T1DM there is an active production of autoantibodies to pancreatic b-cells and the formation of inflammatory infiltrates, the so-called "insulitis" [2]. In connection with the trend towards "rejuvenation" of the age of patients with T1DM, leading to early disability, an increase in the incidence rate, clarification of the mechanisms of immunopathogenesis and the development of new methods for the timely diagnosis of T1DM are relevant.

The key point in the initiation of T1DM is the resistance of autoreactive T lymphocytes to apoptosis. Escape of autoreactive cells from immunological surveillance leads to active destruction of b-cells and subsequent manifestation of the disease [7, 8]. It has been established that in mice of the NOD (nonobese diabetic) line, which are a
