AKT-DRIVEN GLYCOLYSIS CONTRIBUTES TO THE SUPERIOR FUNCTION OF CD137L-DCS, WHOSE DIFFERENTIATION IS MEDIATED BY CD137L AND CD32A

Abstract

Reverse CD137L signaling-induced dendritic cells (CD137L-DCs) are superior to conventional monocyte-derived dendritic cells (moDCs) at polarizing autologous Th1 and Tc1 responses. However, the mechanism of this higher efficacy and CD137L-DC differentiation remains unknown. Using an unbiased screening and metabolic assays, I find higher rates of Akt-driven glycolysis in CD137L-DCs than in moDCs. The inhibition of Akt or glycolysis results in suppression of inflammatory features of mature CD137L-DCs. The differentiation of CD137L-DCs was thought to be mediated solely by CD137L. My data suggest that CD137L interacts with CD32a, both of which are pivotal for reverse CD137L signaling.