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. 2021 Jun 10;12:702726. doi: 10.3389/fimmu.2021.702726

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Copyright © 2021 Scott, Gocher, Workman and Vignali

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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Overview of suppressive mechanisms used by T_regs to create barriers to immune infiltration into tumors. Panel (A) Within the TME, T_regs utilize inhibitory receptors (TIM-3, TIGIT, PD1, and LAG-3), inhibitory cytokines (TGFβ, IL-10, and IL-35), DC modulation (via CTLA-4 and LAG-3), and metabolic disruption (via CD39/CD73) to suppress the anti-tumor T cell response. (B) T_reg-derived TGFβ induces cancer-associated fibroblast (CAF) development that increases extracellular matrix (ECM) production and deposition within the peritumoral space (stroma) to inhibit effector T cell migration. (C) T_regs block entry of effector T cells through preventing proper cytokine signals that promote high endothelial venule (HEV) formation as well as production of inhibitory IL-10 and VEGF to promote dysregulated angiogenesis. (D) In the periphery and secondary lymphoid organs (SLO), T_regs can modulate DC maturity and induce apoptosis to prevent proper effector T cell activation.