ArticleFrontiers in immunology2026
Phospho-enol pyruvate carboxykinase inhibition limits effector function in inflammatory T cells.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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6 authors.
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Abstract
Introduction: Following antigenic stimulation, T cells switch from a catabolic metabolic state maintained by low levels of nutrient uptake to an anabolic metabolism that sustains the biosynthetic and energetic demands of clonal expansion, differentiation, and effector function. Much progress has been made in understanding the transcriptional and enzymatic regulation of activated T cell metabolism. However, less is understood of the role for regulators of anaplerosis and cataplerosis such as phospho-enol pyruvate carboxykinases (PEPCK) in T cells. Methods: Assessment of PEPCK expression in mouse T cells was performed. Pharmacological inhibitors were used to assess functional and metabolic roles for PEPCKs in T cell activation. Results: We show that mitochondrial PEPCK (PEPCK-M) is upregulated following T cell activation, while cytosolic PEPCK-C was not detected. The PEPCK inhibitors limited CD8 Discussion: These data suggest that PEPCKs act to modulate mitochondrial metabolism, supporting effector function in T cells.
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