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. 2020 Dec 21;8(2):e001523. doi: 10.1136/jitc-2020-001523

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© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See http://creativecommons.org/licenses/by-nc/4.0/.

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Natural killer (NK) cells form dynamic interrelationships with immune, stromal and tumor cells with the tumor microenvironment (TME) of head and neck cancer. cDC1, conventional type 1 dendritic cells (DCs). (a) NK cells produce interferon (IFN)-gamma within the TME, which acts on both tumor and neighboring immune cells to enhance antitumor responses. NK cells both recruit cDC1 and provide differentiation and maturation signals for DCs with the TME. (b) Cell–cell interactions between NK cells and neighboring cells determine strength of activation. (c) Cetuximab, monalizumab, and ipilimumab represent some, but not all, monoclonal antibodies that at least in part rely on NK cell activation for full antitumor function. HLA, human leukocyte antigen.