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ATF3 and CH25H regulate effector trogocytosis and anti-tumor activities of endogenous and immunotherapeutic cytotoxic T lymphocytes
Journal article   Open access   Peer reviewed

ATF3 and CH25H regulate effector trogocytosis and anti-tumor activities of endogenous and immunotherapeutic cytotoxic T lymphocytes

Zhen Lu, Noreen McBrearty, Jinyun Chen, Vivek S Tomar, Hongru Zhang, Gianluca De Rosa, Aiwen Tan, Aalim M Weljie, Daniel P Beiting, Zhen Miao, …
Cell metabolism, v 34(9), pp 1342-1358.e7
06 Sep 2022
PMID: 36070682
url
https://doi.org/10.1016/j.cmet.2022.08.007View
Published, Version of Record (VoR) Restricted

Abstract

Immunotherapy Steroid Hydroxylases T-Lymphocytes, Cytotoxic Trogocytosis Virus Replication - genetics
Effector trogocytosis between malignant cells and tumor-specific cytotoxic T lymphocytes (CTLs) contributes to immune evasion through antigen loss on target cells and fratricide of antigen-experienced CTLs by other CTLs. The mechanisms regulating these events in tumors remain poorly understood. Here, we demonstrate that tumor-derived factors (TDFs) stimulated effector trogocytosis and restricted CTLs' tumoricidal activity and viability in vitro. TDFs robustly altered the CTL's lipid profile, including depletion of 25-hydroxycholesterol (25HC). 25HC inhibited trogocytosis and prevented CTL's inactivation and fratricide. Mechanistically, TDFs induced ATF3 transcription factor that suppressed the expression of 25HC-regulating gene-cholesterol 25-hydroxylase (CH25H). Stimulation of trogocytosis in the intratumoral CTL by the ATF3-CH25H axis attenuated anti-tumor immunity, stimulated tumor growth, and impeded the efficacy of chimeric antigen receptor (CAR) T cell adoptive therapy. Through use of armored CAR constructs or pharmacologic agents restoring CH25H expression, we reversed these phenotypes and increased the efficacy of immunotherapies.

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Industry collaboration
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Web of Science research areas
Cell Biology
Endocrinology & Metabolism
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