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. 2022 Feb 9;13:825364. doi: 10.3389/fimmu.2022.825364

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Copyright © 2022 Wang, Zhang, Anderson, Lamble and Orentas

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Bryostatin treatment reveals multiple pathways that CAR-T cells use to eliminate leukemia. In the center of the diagram, pre-B ALL cells are illustrated, displaying the CAR-T target antigen, CD22, innate immune receptor ligands induced by bryostatin that are recognized by activated T cells (Bryostatin-induced NK ligands) and ligands recognized by T cells that have been: a) sensitized by CAR-T production, b) bryostatin-induced, and c) not blocked by cold-target inhibition (CTAK, CAR-T cell non-antigen-specific killing). Also shown are a non-overlapping set of alternative innate immune receptor ligands that are recognized by NK92 upon bryostatin-treatment (right-most effector cell). Cold-target inhibition does not affect NK92 or CD22-specific CAR-T killing. Cold-target does decrease killing evidenced by activated T cells (UTD), but incompletely for CTAK-mediated killing. Green arrows indicate successful cytolysis and blunt red arrow indicates killing impacted by K562-mediated cold target inhibition (classic NK killing).