AMPK drives both glycolytic and oxidative metabolism in murine and human T cells during graft-versus-host disease.

ABSTRACT:

Abstract

Allogeneic T cells reprogram their metabolism during acute graft-versus-host disease (GVHD) in a process involving the cellular energy sensor adenosine monophosphate (AMP)-activated protein kinase (AMPK). Deletion of AMPK in donor T cells limits GVHD but still preserves homeostatic reconstitution and graft-versus-leukemia effects. In the current studies, murine AMPK knock-out (KO) T cells decreased oxidative metabolism at early time points posttransplant and lacked a compensatory increase in glycolysis after inhibition of the electron transport chain. Immunoprecipitation using an antibody specific to phosphorylated targets of AMPK determined that AMPK modified interactions of several glycolytic enzymes including aldolase, enolase, pyruvate kinase M, and glyceraldehyde 3-ph

SUBMITTER: Ramgopal A 

PROVIDER: S-EPMC11345362 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature