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. 2022 Nov 8;15:164. doi: 10.1186/s13045-022-01382-5

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© The Author(s) 2022

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. 6 — Overview of combination non-engineered and engineered NK cell therapies. From top left: in combination with adoptive cell therapy, NK cells are administered with stem cells from a healthy donor. Monoclonal antibodies are combined with NK cells to enhance tumor targeting via antibody-dependent cell cytotoxicity (ADCC) through endogenous CD16 or engineered high-affinity non-cleavable hnCD16 (158 V) on NK cell surface, or as checkpoint inhibitors to block inhibitory receptors on the surface of NK cells (such as programmed cell death protein 1, PD-1) or to block inhibitory ligands on the surface of target cancer cells (such as programmed death-ligand 1, PD-L1). NK cell priming agents, such as IL-15 or IL-15 and IL-15 receptor fusion protein IL-15/IL-15Ra, stimulate NK activation in vivo. NK cell engagers (NKCE) are synthetic molecules built from fragments of monoclonal antibodies engaging simultaneously a tumor-associated antigen (TAA) on the cancer cells and CD16 on the NK cells (e.g., AFM13). Molecular inhibitors act on target cancer cells, inducing apoptosis via inhibition of the proteasome (Bortezomib) or via inhibition of tyrosine kinases (e.g., Imatinib)