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. 2019 Oct 9;9(1):1671763. doi: 10.1080/2162402X.2019.1671763

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© 2019 The Author(s). Published with license by Taylor & Francis Group, LLC.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.

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Figure 1. — Calreticulin and NK cell activation. The exposure of calreticulin (CALR) on malignant blasts from patients with acute myeloid leukemia (AML) favors the accumulation of an activated, poly-functional population of CD11b⁺CD14⁺ myeloid cells that support natural killer (NK) cell anticancer functions. CCR7, C-C motif chemokine receptor 7, IL15RA, interleukin 15 receptor, alpha chain (IL15RA); IFN, interferon.