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Cell Reports Medicine

Cell Reports Medicine

IF: 11.7
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Inhibition of CD38 enzymatic activity enhances CAR-T cell immune-therapeutic efficacy by repressing glycolytic metabolism

Published:20 February 2024 DOI: 10.1016/j.xcrm.2024.101400 PMID: 38307031
Yue Huang,?Mi Shao,?Xinyi Teng,?Xiaohui Si,?Longyuan Wu,?Penglei Jiang,?Lianxuan Liu,?Bohan Cai,?Xiujian Wang,?Yingli Han,?Youqin Feng,?Kai Liu,?Zhaoru Zhang,?Jiazhen Cui,?Mingming Zhang,?Yongxian Hu,?Pengxu Qian,?He Huang

Abstract

Chimeric antigen receptor (CAR)-T therapy has shown superior efficacy against hematopoietic malignancies. However, many patients failed to achieve sustainable tumor control partially due to CAR-T cell exhaustion and limited persistence. In this study, by performing single-cell multi-omics data analysis on patient-derived CAR-T cells, we identify CD38 as a potential hallmark of exhausted CAR-T cells, which is positively correlated with exhaustion-related transcription factors and further confirmed with in?vitro exhaustion models. Moreover, inhibiting CD38 activity reverses tonic signaling- or tumor antigen-induced exhaustion independent of single-chain variable fragment design or costimulatory domain, resulting in improved CAR-T cell cytotoxicity and antitumor response. Mechanistically, CD38 inhibition synergizes the downregulation of CD38-cADPR -Ca2+ signaling and activation of the CD38-NAD+-SIRT1 axis to suppress glycolysis. Collectively, our findings shed light on the role of CD38 in CAR-T cell exhaustion and suggest potential clinical applications of CD38 inhibition in enhancing the efficacy and persistence of CAR-T cell therapy.

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