Vitamin D and autoimmune thyroid diseases (part 2)

The paper is devoted to the disclosure of mechanisms underlying the ability of vitamin D to modulate inflammatory processes in autoimmune thyroid diseases. Vitamin D receptor (VDR) was found to be expressed in many activated immune cells. Calcitriol affects monocytes and dendritic cells by inhibiting the production of inflammatory cytokines, it has effects on differentiation and maturation of antigen-presenting cells, resulting in the suppression of activation and proliferation of T-lymphocytes. Vitamin D was established to be able to shift the differentiation of CD4+ cells towards type 2 T­helpers (Th2) and T­-regulatory phenotypes and inhibit the development and activity of T-helpers of type 17 (Th17) and type 1 (Th1). In recent years, researchers have drawn attention to the regulatory effect of vitamin D on the balance of Treg /Th17 cells. It has been assumed that mutual Th17 and Treg conversion is feasible due to the tight relationship of the processes of differentiation of these cells and presence of the general key development factor — transforming growth factor­β (TGF­β). Proteins of the Smad family play a crucial role in the transmission of TGFβ signals, and Smad3 is important for Treg cells, while Smad7 is associated with the proinflammatory phenotype of T cells. Experiments have established the ability of vitamin D to suppress Smad7 expression, thus promoting increased Smad3 synthesis. Vitamin D has an inhibitory effect on the expression of Th17 cytokines and the differentiation of Th17 cells into pathogenic types. Results of several investigations demonstrated that cholecalciferol preparations had a beneficial effect on thyroid pathology, but these data are ambiguous. Further research is needed to determine the effectiveness of vitamin D intake in the prevention and treatment of autoimmune thyroid disease.