AMPK activation induces RALDH+ tolerogenic dendritic cells by rewiring glucose and lipid metabolism.

ABSTRACT: Dendritic cell (DC) activation and function are underpinned by profound changes in cellular metabolism. Several studies indicate that the ability of DCs to promote tolerance is dependent on catabolic metabolism. Yet the contribution of AMP-activated kinase (AMPK), a central energy sensor promoting catabolism, to DC tolerogenicity remains unknown. Here, we show that AMPK activation renders human monocyte-derived DCs tolerogenic as evidenced by an enhanced ability to drive differentiation of regulatory T cells, a process dependent on increased RALDH activity. This is accompanied by several metabolic changes, including increased breakdown of glycerophospholipids, enhanced mitochondrial fission-dependent fatty acid oxidation, and upregulated glucose catabolism. This metabolic rewiring is funct

SUBMITTER: Brombacher EC 

PROVIDER: S-EPMC11310580 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature