The peptide hormones leptin and ghrelin are func tional antagonists in the energy and fat metabolisms and have multidirectional immunoregulatory activity [1]. These hormones are important for the gestation processes, control of the implantation, and growth and development of the embryo [1]. During the preg nancy, significant changes in fat and energy metabo lisms occur, and dramatic disturbances of fat metabo lism are associated with severe defects of the reproduc tive function [1]. The prerequisite for safe motherhood is the formation of the tolerance of the mother's immune system to fetal antigens [2] caused by the changes in the balance of regulatory subpopulations of T cells, namely, a decrease in the number of IL 17 producing T helpers (Th17) and an increase in the number of T regulatory lymphocytes (Treg) in the peripheral blood. These changes are caused by an increase in the proportion of tolerogenic (immature) dendritic cells (DCs) [3]. DCs are the main antigen presenting cells which produce a wide range of cytok ines, depending on the maturation stage and the acti vation conditions; they also determine the differentia tion of naive CD4 + T cells and the type of adaptive immune response [4]. Immature DCs produce tolero genic cytokines, such as interleukin (IL) 10 and trans forming growth factor β1 (TGF β1), thus activating the formation of adaptive (a) Treg and induce immune tolerance [4]. The hormones and cytokines such as IL 10 and TGF β1 can stabilize the tolerogenic capacity of immature DCs [2][3][4]. Thus, the study of the factors affecting the DC maturation and CD4 + T cell differentiation is important for the understanding of the mechanisms controlling the immune response direction and the formation of the peripheral toler ance during pregnancy.The goal of this study was to investigate the effects of leptin and ghrelin, as well as their combinations at concentrations corresponding the levels of these hor mones in peripheral blood during pregnancy, on DC maturation and the induction by these hormones of the regulatory subpopulations of T cells.
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