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Immunogenetic metabolomics revealed key enzymes that modulate CAR-T metabolism and function [RNA-seq]

ABSTRACT: Immunogenetic metabolomics revealed key enzymes that modulate CAR-T metabolism and function [RNA-seq]

PROVIDER: PRJNA934482 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23440885_1.fastq.gz	Fastqsanger.gz
	SRR23440885_2.fastq.gz	Fastqsanger.gz
	SRR23440886_1.fastq.gz	Fastqsanger.gz
	SRR23440886_2.fastq.gz	Fastqsanger.gz
	SRR23440887_1.fastq.gz	Fastqsanger.gz

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Immunogenetic metabolomics revealed key enzymes that modulate CAR-T metabolism and function

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Project description:Immunogenetic metabolomics revealed key enzymes that modulate CAR-T metabolism and function [DNA-edit]

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Immunogenetic metabolomics revealed key enzymes that modulate CAR-T metabolism and function [DNA-edit]

Project description:Immune evasion is a critical step of cancer progression that remains a major obstacle for current T cell-based immunotherapies. Hence, we seek to genetically reprogram T cells to exploit a common tumor-intrinsic evasion mechanism, whereby cancer cells suppress T cell function by generating a metabolically unfavorable tumor microenvironment (TME). Specifically, we use an in silico screen to identify ADA and PDK1 as metabolic regulators, in which gene overexpression (OE) enhances the cytolysis of CD19-specific CD8 CAR-T cells against cognate leukemia cells, and conversely, ADA or PDK1 deficiency dampens such effect. Additionally, ADA-OE in CAR-T cells improves cancer cytolysis under high concentrations of adenosine, the ADA substrate and an immunosuppressive metabolite in the TME. High-throughput transcriptomics and metabolomics in these CAR-Ts reveal alterations of global gene expression and metabolic signatures in both ADA- and PDK1- engineered CAR-T cells. Functional and immunological analyses demonstrate that ADA-OE increases proliferation and decreases exhaustion in α-CD19 and α-HER2 CAR-T cells. We then show ADA-OE improves tumor infiltration and clearance by α-HER2 CD4 and CD8 CAR-T with an in vivo colorectal cancer model. Collectively, these data unveil systematic knowledge of metabolic reprogramming directly in CAR-T cells, and reveal potential targets for improving CAR-T based cell therapy.

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Immunogenetic metabolomics revealed key enzymes that modulate CAR-T metabolism and function [RNA-seq]

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Immunogenetic metabolomics revealed key enzymes that modulate CAR-T metabolism and function.

Project description: Not available

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Immunogenetic metabolomics revealed key enzymes that modulate CAR-T metabolism and function

Project description:This SuperSeries is composed of the SubSeries listed below.

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CAR-adapted PIK3CD base editing enhances T cell anti-tumor potency

Project description:Insufficient functional T cell persistence impedes therapeutic success of chimeric antigen receptor (“CAR”) therapies. Here, we performed a CAR-adapted base editing screen of PIK3CD, a key regulator of T cell function, metabolism, and fate. We identified point mutations that beneficially modulate CAR T cell profiles in 4-1BBz and 28z CAR T cells, respectively. Remarkably, point mutations with differing effects on PI3Kδ signaling activity were advantageous in distinct CAR contexts: The PI3Kδ-activating mutation E81K enhanced proliferation, metabolic fitness and effector function in 4-1BBz CARs, promoting long-term functional persistence and enhanced therapeutic efficacy in vivo. Conversely, the PI3Kδ-attenuating mutation L32P improved T cell memory formation and functionality in 28z CAR T cells. Together, our approach of Rational Optimization of Activation-dependent Signaling via Targeted Allelic Reprogramming (ROADSTAR) illustrates the importance of CAR design-specific fine-tuning of tailoring intrinsic T cell signaling and demonstrates the potential of base editing for next-generation cellular therapies.

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