Inhibitory receptors PD-1, TIM-3, LAG-3, etc. – “immune checkpoints” – are expressed by activated effector T cells in order to limit the intensity of the immune response. Under the conditions of chronic infectious process and tumor growth, checkpoint receptors are expressed by T lymphocytes in a state of T cell exhaustion, characterized by a decrease in its proliferative, cytotoxic and cytokine-producing activity. Restoring the functional activity of T cells underlies the mechanism of action of therapeutic monoclonal antibodies – “checkpoint inhibitors”, such as anti-PD-1/PD-L1 and antiLAG-3 used in antitumor therapy. At the same time, checkpoint receptors are expressed by multiple cell populations, including regulatory T cells (T-regs), which suppress immune response. Data on the functions of inhibitory receptors on T-reg continue to be studied. In this article, we provide the recent knowledge on T-reg populations’ expression of inhibitory checkpoint receptors and how these relate to checkpoint inhibitor therapy’s outcomes.