Acetate for memory

Systemic concentrations of acetate increase in metabolic-stress conditions, such as starvation and pathogen infection. In Immunity, Hess and colleagues show that increased concentrations of extracellular acetate during bacterial infection are required for optimal responses of CD8⁺ T_mem cells. Bacterial infection in mice triggers the release of acetate into the systemic circulation, and in vitro exposure of T_mem cells to acetate concentrations similar to those found during early infection enhances their production of IFN-γ, glycolytic reserve and spare respiratory capacity. Exogenous acetate is metabolized into acetyl-CoA and promotes acetylation of the glycolytic enzyme GAPDH in T_mem cells. This post-translational modification is required for GAPDH's enzymatic function and IFN-γ production. In vivo treatment with acetate increases the glucose metabolism and production of IFN-γ in CD8⁺ T_mem cells during reactivation, while the transfer of acetate-exposed CD8⁺ T_mem cells controls bacterial infection better than the transfer of untreated cells does.

Immunity (17 May 2016) doi:10.1016/j.immuni.2016.03.016