Serotonin is involved in the regulation of a wide range of immune system functions in sexually mature animals. It was previously shown that the suppression of serotonin synthesis in fetuses during the formation of the thymus leads to long-term irreversible changes in the functioning of the T-system immunity. However, the mechanisms of morphogenetic influence of serotonin on the development of the thymus remain unclear. In this study, the expression of mRNA and the protein product of serotonin receptor type 1A (Htr1a) in the fetal thymus was revealed. A single administration of the Htr1a antagonist NAN-190 into fetuses in utero on the 17th day of embryonic development caused a persistent increase in the functional activity of T-lymphocytes in postnatal life. Research on the model of the organotypic culture of the embryonic thymus shows that the Htr1a blockade accelerates the differentiation of T-lymphocytes at the earliest stages of their development and has little effect on the formation of mature forms of T-helper cells and cytotoxic T‑lymphocytes. The presence of Htr1a receptors in the developing thymus confirms the possibility of a direct influence of serotonin on the formation of this organ. It was found that serotonin can act through Htr1a and can change the balance of cytokines in the forming thymus, which may underlie the mechanisms of ontogenetic plasticity of the immune system. Cytokines that are responsible for differentiation of thymus cell elements appear to be one of the key links through which the morphogenetic effect of serotonin mediated by activation of the Htr1a receptor is realized.