Nancie J. MacIver

TL;DR: Teff and Treg were selectively increased in Glut1 transgenic mice and reliant on glucose metabolism, whereas Treg had activated AMP-activated protein kinase and were dependent on lipid oxidation.

TL;DR: The role of cellular metabolism in T cell development, activation, differentiation, and function is discussed to highlight the clinical relevance and opportunities for therapeutic interventions that may be used to disrupt immune pathogenesis.

TL;DR: It is shown that glucose uptake is limiting in T cell activation and that CD28 costimulation is required to allow maximal glucose uptake following TCR stimulation by up-regulating expression and promoting the cell surface trafficking of the glucose transporter Glut1.

TL;DR: In this article, the authors evaluated CD4+ T cell populations in murine models and determined that inflammatory T cells maintain high expression of glycolytic genes, while Tregs are oxidative and require mitochondrial electron transport to proliferate and differentiate.

TL;DR: Understanding of the signals that regulate the expression and localization of glucose transporter 1 (Glut1) to allow glucose uptake in T cells are beginning to be understood and may lead to therapeutic strategies to target some forms of cancer or autoimmunity.