Abstract
A shift in the energy-metabolism balance from oxidative phosphorylation to glycolysis is observed in several phenomena, from oncogenesis to differentiation. And this shift is not merely an indicator of the phenotypic change-an increase in glucose delivery often drives the adaption. At first blush, it seems that any route of entry should be equivalent, as long as sufficient quantities are supplied. However, an extensive study comparing the Th17 and Th1 subtypes of T cells now suggests that similar glucose transporters may not be interchangeable. Manipulation of individual transporters, or the downstream metabolites of their substrates, may afford dampening of autoimmunity potential with some degree of precision.