A DETAILED ANALYSIS OF THE LITERATURE ON THEPATHOGENETIC FEATURES OF HASHIMOTO'S AUTOIMMUNETHYROIDITISTHE

Abstract

Hashimoto's autoimmune thyroiditis (AIT) is a chronic inflammatory disease of the thyroid gland (TG) of autoimmune genesis, in which chronic progressive lymphoid infiltration occurs as a result of impaired tolerance to thyroid autoantigens, followed by gradual destruction of the thyroid parenchyma with a 70-80% probability of transition to primary hypothyroidism. Together with Graves' disease, it is the most common autoimmune thyroid disease. This disease is multifactorial - both genetic predisposition and environmental factors contribute to its
development. Over the past 20 years, the prevalence of AIT has increased more than 10-fold. To systematize and analyze the material of recent studies on the molecular mechanisms of the pathogenesis of Hashimoto's autoimmune thyroiditis. The study uses analytical and bibliosemantic methods. Hashimoto's autoimmune thyroiditis is a chronic inflammatory disease of the thyroid gland of autoimmune genesis, in which chronic progressive lymphoid infiltration occurs as a result of impaired tolerance to thyroid autoantigens, followed by gradual destruction of the thyroid parenchyma. The disease is more commonly observed at the age of 45-65 years and is multifactorial - both genetic predisposition and environmental factors contribute to its development. The ratio of female to male patients is approximately 10-20:1, and in recent years the prevalence of Hashimoto's autoimmune thyroiditis has increased more than 10 times. On
morphologic examination, the thyroid gland is diffusely enlarged, the surface of the incision is pale, yellow-brown, dense and nodular. Microscopic examination of the parenchyma reveals
numerous large mononuclear inflammatory infiltrates consisting of small lymphocytes and plasma cells and well-formed germinal centers. The twin method is used to assess the degree of contribution of genetic and environmental factors. Studies have shown significantly greater concordance in monozygotic twins than in dizygotic twins, which confirms the important role of genetic factors in the etiology. The main immune mechanisms of damage include direct action of cytotoxic CD8+ T cells on thyrocytes by binding through the Fas receptor - Fas ligand system; the effect of cytokines, in particular, interferon γ, which is produced by TH1 cells and leads to macrophage activation with subsequent follicular damage, antibody-dependent cellmediated cytotoxicity, in which Fc fragments of antibodies pre-bound to thyrocytes are binding
sites for killing cells, in particular, NK cells. In terms of thyroid cell damage, cytokines produced by the lymphocyte infiltrate play a key role. These include differentiation, signal transduction, and stimulation of other cells to release proinflammatory mediators or synthesize antibodies. It is worth noting their ability to stimulate the thyroid cells themselves to release
inflammatory mediators, thereby enhancing and consolidating the autoimmune process. Researchers have identified other mechanisms, and the ratio of their contribution to the development of the overall pathological process is a matter of debate and may differ from
patient to patient. One of the explanations may be the multifactorial nature of the disease, in particular, different genetic mutations can lead to different disorders of intracellular and intercellular signaling, but the resultant factor will be the same - immune autoaggression. The
pathogenesis of Hashimoto's autoimmune thyroiditis is complex and multifaceted, involving both humoral and cellular immunity. The disease can be triggered by a mutation in the mechanisms of immune regulation, a mutation in the cells of the thyroid gland itself, and environmental factors.