title: Starved human T lymphocytes keep fighting.
abstract: Cellular metabolism is emerging as a key determinant of T-lymphocyte differentiation and function. While this new paradigm has been primarily characterized in murine systems, research is now characterizing a role for different aspects of cellular metabolism in controlling human T-lymphocyte biology. In this issue of the European Journal of Immunology, Renner et al. [Eur. J. Immunol. 2015. 45: 2504-2516] analyze the glycolytic and mitochondrial activity of activated human CD4(+) and CD8(+) T cells, and correlate it to T-cell function. The authors show that although neither glucose deprivation nor mitochondrial restriction affects cytokine production, the glycolytic inhibitor 2-deoxyglucose severely affects T-cell function.
authors.affiliation: School of Biochemistry and Immunology and School of Pharmacy and Pharmaceutical Sciences, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin 2, Ireland.
authors.forename: David K
authors.initials: DK
authors.lastname: Finlay
mesh_terms: D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism*; D018414:CD8-Positive T-Lymphocytes / Q000378:metabolism*; D003847:Deoxyglucose / Q000494:pharmacology*; D005947:Glucose / Q000172:deficiency*; D006801:Humans; D008928:Mitochondria / Q000378:metabolism*; D016176:T-Lymphocyte Subsets / Q000378:metabolism*
chemical_list: D003847:Deoxyglucose; D005947:Glucose
keywords: Cytokines; Glucose deprivation; Human T cells; Metabolism; Mitochondria