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. 2020 Aug 12;13:111. doi: 10.1186/s13045-020-00947-6

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — CTLA-4-mediated immune regulation. Schematic illustrating T cell-intrinsic (left) and extrinsic regulation by CTLA-4 (right). Left: CTLA-4 is upregulated on activated T cells and competes with the CD28 co-stimulatory receptor due to its higher affinity for CD80/CD86. Right: CTLA-4 plays a critical role in Treg-mediated immune regulation. The CTLA-4/CD80 interaction between Treg/APCs induces indoleamine 2,3-dioxygenase (IDO), a key enzyme that suppresses T cells by tryptophan deprivation. Additionally, Tregs down-modulate CD80/86 expression on APCs by transendocytosis