The Role of T-Regulatory Cells in the Control and Induction of Inflammation

In recent years, regulatory T cells (Treg), which are important for maintaining immune tolerance, controlling the immune response against self-antigens, allergens, pathogens and tumors, have been actively studied. Epigenetic changes can impart a fairly stable pattern of gene expression to Treg cells producing suppressor cytokines IL-10, TGF-β and IL-35, and inhibitory molecules CTLA-4, PD, Lag-3, TIGIT, CD73 and CD39. At the same time, Treg cells are a plastic and dynamic population dependent on epigenetic factors and microenvironment. Long-term stimulation with antigen in chronic infections induces exhaustion of T cells, which lose effector functions with a decrease in the secretion of IFN-γ, TNF-α and IL-2 and the acquisition of suppressor potential. Under certain conditions, expression of the transcription factor Foxp3 in Treg cells decreases, which leads to a loss of suppressor activity and is accompanied by their differentiation into memory T cells capable of maintaining chronic inflammation. Quite often, infectious pathogens increase the activity of Treg cells to weaken the immune response against them, which can provoke the development of autoimmune diseases. Treg cells function in various non-lymphoid tissues to prevent inflammation and immune pathology. In addition, Treg cells can perform “non-canonical” functions in non-lymphoid organs that are associated with tissue development and their homeostasis. An important mechanism of protective and pathogenic action turned out to be extracellular vesicles secreted by Treg cells containing molecules that are specifically delivered to recipient cells to regulate functions. Thus, Treg cells are involved not only in the control, but also in the induction of acute and chronic immune inflammation. In this regard, approaches to the development of fundamentally new methods for the diagnosis and treatment of autoimmune, infectious and tumor diseases are of particular interest.