[HTML][HTML] Metabolic pathways in T cell activation and lineage differentiation

L Almeida, M Lochner, L Berod, T Sparwasser - Seminars in immunology, 2016 - Elsevier
L Almeida, M Lochner, L Berod, T Sparwasser
Seminars in immunology, 2016Elsevier
Recent advances in the field of immunometabolism support the concept that fundamental
processes in T cell biology, such as TCR-mediated activation and T helper lineage
differentiation, are closely linked to changes in the cellular metabolic programs. Although the
major task of the intermediate metabolism is to provide the cell with a constant supply of
energy and molecular precursors for the production of biomolecules, the dynamic regulation
of metabolic pathways also plays an active role in shaping T cell responses. Key metabolic …
Abstract
Recent advances in the field of immunometabolism support the concept that fundamental processes in T cell biology, such as TCR-mediated activation and T helper lineage differentiation, are closely linked to changes in the cellular metabolic programs. Although the major task of the intermediate metabolism is to provide the cell with a constant supply of energy and molecular precursors for the production of biomolecules, the dynamic regulation of metabolic pathways also plays an active role in shaping T cell responses. Key metabolic processes such as glycolysis, fatty acid and mitochondrial metabolism are now recognized as crucial players in T cell activation and differentiation, and their modulation can differentially affect the development of T helper cell lineages. In this review, we describe the diverse metabolic processes that T cells engage during their life cycle from naļve towards effector and memory T cells. We consider in particular how the cellular metabolism may actively support the function of T cells in their different states. Moreover, we discuss how molecular regulators such as mTOR or AMPK link environmental changes to adaptations in the cellular metabolism and elucidate the consequences on T cell differentiation and function.
Elsevier