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According to recent data, vitamin D is classified as a substance with hormonal activity, which, in addition to classical, has “non-classical” effects caused by the complex relationship between vitamin D and effector cells of the immune system. This relationship is based on the expression of the vitamin D receptor (VDR) on immune cells, which is encoded by the corresponding VDR gene. Vitamin D receptor specifically binds the active form of vitamin D (1,25(OH)2D3). As a result, a D3-VDR complex is formed, which mediates the effects of vitamin D through the formation of intracellular signaling pathways that transform the activity of certain target genes. However, it is not entirely clear how vitamin D realizes its effects at the cellular and receptor levels. According to the literature, studies of recent decades have revealed a significant role of vitamin D and immune checkpoint receptors (PD-1 (programmed cell death), PD-L (PD ligand), CTLA (cytotoxic T lymphocyte associated protein)) in autoimmune diseases. This review outlines possible mechanisms for the interconnection of these pathways. A deeper understanding of the intercellular interactions mediated by ligand-associated activation of vitamin D receptors, D3-VDR complex and immune checkpoint receptors (PD-1, PD-L, CTLA) in inflammation may become the basis for the development of new strategies for the diagnosis, prognosis and treatment of various diseases
Ablyakimov et al. (Mon,) studied this question.