Metabolic reprogramming in memory T cells

Metabolic reprogramming in memory T cells

Lab Pearce

Figure 1 In response to antigen and costimulation, T cells become activated, proliferate, and gain effector functions important for clearing pathogens or tumors. Long-lived memory T cells are also generated during an immune response and are important for protecting the host against future re-infection. T cells must adapt to a wide array of environmental stressors as part of their normal development and undergo dramatic metabolic remodeling in the process.

T cells are maintained in fairly constant numbers, but upon activation undergo a developmental program characterized by distinct phases encompassing the expansion and then contraction of antigen-specific effector T cells, followed by the persistence of long-lived memory T cells. Although this predictable pattern of a T cell response is well established, the mechanisms regulating how T cells generate these different fates are not well understood (Figure 1).

Our work has shown that specific metabolic programs must be in place to support the development of memory T cells. We have found that memory T cells rely on mitochondrial metabolism, and in particular, require the oxidation of intracellular fatty acids for development. New work in our lab is focused on how mitochondrial phenotype and morphology dictate metabolic pathway engagement and as such enforces either the effector or memory fate of a T cell.

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