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. 2021 Sep 16;9(9):e003149. doi: 10.1136/jitc-2021-003149

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© Author(s) (or their employer(s)) 2021. 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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CD33 chimeric antigen receptor construct (CD33CART) inhibits acute myeloid leukemia (AML) proliferation in vivo. (A) Luciferase-transduced MOLM14 cells (1×10⁶) were injected intravenously via tail vein into NSG mice on day 0. Once engraftment was documented by bioluminescent imaging (BLI) on day 7, cohorts of three mice were randomized to intravenous treatment with saline, GFP-transduced T cells ((-)TC), or one of the CD33CARTs as designated (5×10⁶ total cells/mouse; red arrow). Mice were followed by weekly BLI and euthanized when a predetermined maximal radiance level of 1×10⁶ photons/s/cm²/sr was detected, indicative of leukemia progression. All three gemtuzumab-based (gem), lintuzumab-based (lin), and M195-based CD33CARTs demonstrated some anti-leukemia activity in vivo with complete inhibition of MOLM14 proliferation observed only in the 4-1BB/CD3ζ (BBz) construct-containing T cells versus partial activity with CD28/CD3ζ(28z) versions. (B) Graphic representation of summary BLI radiance data was performed in Prism. 28z, CD28/CD3ζ endodomains, BBz, 4–1BB/CD3ζ endodomains.