NEW ASPECTS OF IMMUNOPATHOGENESIS OF GRAVES’ DISEASE – CYTOKINES REGULATION AND CELLULAR INFILTRATION OF A THYROID GLAND AT AN AUTOIMMUNE THYROTOXICOSIS

It is revealed that significant changes in serum levels of a number of opposed cytokines with a significant increase of IFN-γ and IL-2 on the background of TGF-β1 deficiency initially and on the background of thiamazole therapy, which indicates Tregs dysfunction followed by a depletion phenomenon occur in Graves’ disease. Preservation of elevated IL-10 levels on the background of 6 months of thyrotoxicosis therapy indicates a negative role of the cytokine due to the well-known induction of Treg diff erentiation into Th17 cells with subsequent reduction in the number of Tregs. Along with the study of thyroid hormones, TSH and thyroid autoantibodies, it is advisable to monitor the serum levels of IL-2, IFN-γ, IL-6, sIL-6R, IL-17 and TGF-β1, initially and during the thiamazole therapy for adequate monitoring of the autoimmune process and prediction of a possible recurrence of the disease, including when deciding on the radical treatment. The study obtained convincing data on the participation of mastocytes in the pathogenesis of Graves’ disease, but not in the nodal euthyroid goiter. The active migration of mast cells to the thyroid gland in Graves’ disease, their degranulation in the intra- and interfollicular space and their expression of CD86 predetermines the ability of mast cells to participate in the antigen-presenting function in autoimmune thyrotoxicosis, which opens up prospects for personalized pathogenetic therapy of the disease.