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Genetic engineering of T cells with chimeric T-cell receptors (CARs) is an attractive strategy to treat malignancies. It extends the range of antigens for adoptive T-cell immunotherapy, and major mechanisms of tumor escape are bypassed. With this strategy we redirected immune responses towards the CD33 antigen to target acute myeloid leukemia. To improve  in vivo  T-cell persistence, we modified human Epstein Barr Virus-(EBV-) specific cytotoxic T cells with an anti-CD33.CAR. Genetically modified T cells displayed EBV and HLA-unrestricted CD33 bispecificity  in vitro . In addition, though showing a myeloablative activity, they did not irreversibly impair the clonogenic potential of normal CD34 +  hematopoietic progenitors. Moreover, after intravenous administration into CD33 +  human acute myeloid leukemia-bearing NOD-SCID mice, anti-CD33-EBV-specific T cells reached the tumor sites exerting antitumor activity  in vivo . In conclusion, targeting CD33 by CAR-modified EBV-specific T cells may provide additional therapeutic benefit to AML patients as compared to conventional chemotherapy or transplantation regimens alone.

advances in hematology

<i>In Vitro</i>and<i>In Vivo</i>Antitumor Effect of Anti-CD33 Chimeric Receptor-Expressing EBV-CTL against<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:msup><mml:mrow><mml:mtext>CD</mml:mtext><mml:mn mathvariant="bold">33</mml:mn></mml:mrow><mml:mrow><mml:mo mathvariant="bold">+</mml:mo></mml:mrow></mml:msup></mml:math>Acute Myeloid Leukemia

In VitroandIn VivoAntitumor Effect of Anti-CD33 Chimeric Receptor-Expressing EBV-CTL againstCD33+Acute Myeloid Leukemia