Effector and memory T cells show differences in their metabolic states and use of energy sources. In Immunity, Pearce and colleagues explore how CD8+ T cells switch their metabolic state to become memory cells. Unlike glycolytic effector cells, memory CD8+ T cells use oxidative phosphorylation to generate ATP. Stimulation with IL-15 triggers more mitochondrial spare respiratory capacity (reflected by more oxygen consumption), but stimulation with IL-2 does not. These changes are correlated with more biogenesis of mitochondria, as more mitochondria are found in memory cells than in naive or effector CD8+ T cells. IL-15 induces upregulation of CPT1, a rate-limiting enzyme that allows the cells to use fatty acids as an energy source. Modulation of CPT1 alters the generation of memory cells in vitro and, notably, in vivo in response to infection with Listeria monocytogenes. Thus, IL-15 contributes to memory development by regulating mitochondrial abundance and function.

Immunity 36, 1–11 (2012)