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The mitochondrial pyruvate carrier regulates antitumor function and memory T cell differentiation

ABSTRACT: The mitochondrial pyruvate carrier regulates antitumor function and memory T cell differentiation

PROVIDER: PRJNA765936 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16039611_1.fastq.gz	Fastqsanger.gz
	SRR16039611_2.fastq.gz	Fastqsanger.gz
	SRR16039612_1.fastq.gz	Fastqsanger.gz
	SRR16039612_2.fastq.gz	Fastqsanger.gz
	SRR16039613_1.fastq.gz	Fastqsanger.gz

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The mitochondrial pyruvate carrier regulates antitumor function and memory T cell differentiation

Project description:Effector CD8+ T cells engage glycolysis for both lactate fermentation and pyruvate oxidation, the latter requiring the mitochondrial pyruvate carrier (MPC). How mitochondrial pyruvate metabolism impacts T cell function and fate, remains incompletely understood. We found that genetic deletion of MPC drives CD8+ T cell differentiation towards a memory phenotype. Metabolic flexibility induced by MPC inhibition in a nutrient-rich environment allowed for increased acetyl-coenzyme-A production by glutamine and fatty acid oxidation. This correlated with histone acetylation and chromatin accessibility on pro-memory genes. However, in a nutrient-deprived tumor microenvironment, MPC is essential for sustaining lactate oxidation that limits the metabolic suppression of CD8+ T cell anti-tumor function. To optimally translate these findings, we used a small molecule MPC inhibitor to imprint a stable memory phenotype during chimeric antigen receptor (CAR) T manufacturing, and demonstrated that infusing metabolically conditioned MPC WT CAR T cells resulted in superior and long-lasting anti-tumor activity.

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Mitochondrial Pyruvate Carrier 1 (MPC1) enforces T cell homeostasis by enabling pyruvate oxidation in the mitochondria

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