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. 2021 Jan 15;11:585819. doi: 10.3389/fimmu.2020.585819

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Copyright © 2021 Bayati, Mohammadi, Valadi, Jamshidi, Foma and Sharif-Paghaleh

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Cell-mediated suppression mechanisms of Tregs. A variety of molecular mechanisms might operate in a complementary fashion to contribute to Treg-mediated suppression. Tregs exert these suppressive effects on different cell types mainly via three mechanisms: 1) Producing soluble factors such as anti-inflammatory cytokines (IL-10, IL-35, and TGF-β), FLG-2, adenosine, granzyme and perforin. 2) Competing for growth factors: high-affinity CD25 receptors on Tregs and effector T cells compete for the relating ligands.3) Inhibitory receptors: Tregs have been observed to have a direct effect on target cells via interaction of CTLA-4, TIM-3, NRP-1, Gal-1 and LAG-3 and their ligands. CTLA-4, cytotoxic T lymphocyte-associated antigen-4; DC, dendritic cell; FLG-2, fibrinogen-like protein-2; GAL-1, Galectin-1; LAG3, lymphocyte activation gene 3; TGF, transforming growth factor; Treg , regulatory T cell; Teff, effector T cells; TIM-3, T cell immunoglobulin and mucin domain 3; Th17, T helper17; Nrp-1, Neuropilin; MQ, macrophage; IL-2, Interleukin-2; IL-6, Interleukin-6; IL-10, Interleukin-10; IL-35, Interleukin-35.