PD-1 signaling affects cristae morphology and leads to mitochondrial dysfunction in human CD8+ T lymphocytes

Abstract

Our results suggest that mitochondria are the main targets of PD-1 inhibitory activity. PD-1 reprograms CD8⁺ T cell metabolism for efficient use of fatty acid oxidation; this mitochondrial phenotype might explain the long-lived phenotype of PD-1-engaged T cells.