We studied the ability of melatonin in physiological and pharmacological concentrations to induce and/or regulate differentiation of T cells producing IL-17 (Th17). This hormone produced the opposite effect on CD4+T cells, which depended on their activation status. Melatonin induced the synthesis of IL-17A by intact T cells, but had little effect on activated cells. Melatonin in high (pharmacological) concentration decreased the intracellular expression of this cytokine under conditions of polyclonal activation. Melatonin had a dose-depended effect. Taking into the fact that Th17 cells play an important role in the immune defense, it can be suggested that the regulation of their activity by melatonin contributes to this process.
We studied the role of endogenous melatonin in the development and functioning of T cells that produce IL-17 (Th17) and regulatory T cells (Treg) during pregnancy. The study was performed ex vivo and in vitro with auto-serum as the source of endogenous melatonin under conditions of blockade of melatonin-dependent signaling. Participation of the hormone in the regulation of differentiation of both CD4RORγt and CD4FoxP3T cells and their key products IL-17A and TGF-β was demonstrated. It is known that the normal gestational process is accompanied by a decrease in Th17/Treg ratio due to hormonal changes. The sensitivity of the studied subpopulations to melatonin during pregnancy can affect its outcome.
The expression of class IV semaforin Sema4D and its CD72 receptor on lymphocytes was studied in patients with multiple sclerosis. The disease was associated with an increase in Sema4D level on intact T lymphocytes and with its more intense shedding from the membrane of activated cell. Multiple sclerosis was also associated with a decrease of CD72 receptor expression by B lymphocytes. Possible contribution of Sema4D to the disease development via the direct effects in the CNS and the immunomodulatory effect, specifically, B cell activity regulation, was discussed.
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