Fueling memories

Abstract

A hallmark of the adaptive immune response is rapid and robust activation upon rechallenge. In the current issue of Immunity, van der Windt et al. (2012) provide an important link between mitochondrial respiratory capacity and the development of CD8(+) T cell memory.

Figure. Metabolic view of CD8+ effector versus memory cells

From an immunologic perspective, upon activation CD8+ effector cells are short lived killers able to rapidly proliferate and secrete cytokines. Memory cells on the other hand are long lived cells circulating throughout the lymphoid tissue. Upon activation however, they too rapidly proliferate, secrete cytokines and kill targets. The work of van der Windt et al. paints a contrasting metabolic portrait of these two cell types. IL-2-promoted effector cells employ primarily glucose for fuel and aerobic glycolysis for energy and raw materials. IL-15 promoted memory cells demonstrate increased mitochondrial mass, employ oxidative phosphorylation and fatty acid oxidation with increased expression of of CPT1a. Overall this results in an increase in spare respiratory capacity, an increase in ATP and a decrease in superoxide generation. The net result is that memory cells are built for long term survival and poised for secondary rechallenge.