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

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.

Overexpression of AMPKγ2 increases AMPK signaling to augment human T cell metabolism and function.

Cellular therapies are currently employed to treat a variety of disease processes. For T cell-based therapies, success often relies on the metabolic fitness of the T cell product, where cells with enhanced metabolic capacity demonstrate improved in vivo efficacy. AMP-activated protein kinase (AMPK) is a cellular energy sensor which combines environmental signals with cellular energy status to enforce efficient and flexible metabolic programming.

Enhanced visible-light photocatalytic activity of perylene diimide (PDI) supramolecular nanorods with Pt QDs deposited in situ.

Well-dispersed Pt quantum dots (QDs) were the first to be successfully deposited onto a PDI supramolecular nanorods surface via a simple in situ chemical reduction. Under visible light irradiation, Pt QDs/PDI composites displayed excellent photocatalytic property in the degradation of phenol. The optimum 1 wt% Pt QDs/PDI composite was found to be 6.