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Venetoclax enhances T cell–mediated antileukemic activity by increasing ROS production

Published:22 July 2021 DOI: 10.1182/blood.2020009081 PMID: 34292323
Jong Bok Lee,?Dilshad H Khan,?Rose Hurren,?Mingjing Xu,?Yoosu Na,?Hyeonjeong Kang,?Sara Mirali,?Xiaoming Wang,?Marcela Gronda,?Yulia Jitkova,?Neil MacLean,?Andrea Arruda,?Zoe Alaniz,?Marina Y Konopleva,?Michael Andreeff,?Mark D Minden,?Li Zhang,?Aaron D Schimmer

Abstract

Venetoclax, a Bcl-2 inhibitor, in combination with the hypomethylating agent azacytidine, achieves complete remission with or without count recovery in ~70% of treatment-naive elderly patients unfit for conventional intensive chemotherapy. However, the mechanism of action of this drug combination is not fully understood. We discovered that venetoclax directly activated T cells to increase their cytotoxicity against acute myeloid leukemia (AML) in vitro and in vivo. Venetoclax enhanced T-cell effector function by increasing reactive oxygen species generation through inhibition of respiratory chain supercomplexes formation. In addition, azacytidine induced a viral mimicry response in AML cells by activating the STING/cGAS pathway, thereby rendering the AML cells more susceptible to T cell-mediated cytotoxicity. Similar findings were seen in patients treated with venetoclax, as this treatment increased reactive oxygen species generation and activated T cells. Collectively, this study presents a new immune-mediated mechanism of action for venetoclax and azacytidine in the treatment of AML and highlights a potential combination of venetoclax and adoptive cell therapy for patients with AML.

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