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. 2020 Dec 7;13:167. doi: 10.1186/s13045-020-00996-x

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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 — Mechanisms of immune escape from NK cell-mediated recognition in AML. Dysfunctional NK cells exhibit an imbalanced receptor expression with the overexpression of inhibitory receptors and the underexpression of activating receptors. AML cells display a defective expression of cognate ligands for NK cell activating and inhibitory receptors. The tumor microenvironment consisting of Treg cells and MDSCs can interfere with the function of NK cells through the secreting of cytokines. MDSC myeloid-derived suppressor cell, NK natural killer cell; Treg regulatory T cell