title: Does metabolic reprogramming underpin age-associated changes in T cell phenotype and function?
abstract: T cells are required for an effective adaptive immune response. The principal function of T cells is to promote efficient removal of foreign material by identifying and mounting a specific response to nonself. A decline in T cell function in aging is thought to contribute to reduced response to infection and vaccination and an increase in autoimmunity. This may in part be due to the age-related decrease in naïve CD4(+) T cells and increase in antigen-experienced CD4(+) T cells, loss of redox homeostasis, and impaired metabolic switching. Switching between subsets is triggered by the integration of extracellular signals sensed through surface receptors and the activation of discrete intracellular metabolic pathways. This article explores how metabolic programming and loss of redox homeostasis during aging may contribute to age-associated changes in T cell phenotype and function.
authors.affiliation: Life and Health Sciences and Aston Research Centre for Healthy Ageing, Aston University, Birmingham B4 7ET, West Midlands, UK.
authors.forename: Rita C
authors.initials: RC
authors.lastname: Torrão
authors.affiliation: Life and Health Sciences and Aston Research Centre for Healthy Ageing, Aston University, Birmingham B4 7ET, West Midlands, UK.
authors.forename: Stuart J
authors.initials: SJ
authors.lastname: Bennett
authors.affiliation: Life and Health Sciences and Aston Research Centre for Healthy Ageing, Aston University, Birmingham B4 7ET, West Midlands, UK.
authors.forename: James E
authors.initials: JE
authors.lastname: Brown
authors.affiliation: Life and Health Sciences and Aston Research Centre for Healthy Ageing, Aston University, Birmingham B4 7ET, West Midlands, UK. Electronic address: h.r.griffiths@aston.ac.uk.
authors.forename: Helen R
authors.initials: HR
authors.lastname: Griffiths
mesh_terms: D056704:Adaptive Immunity / Q000235:genetics; D000375:Aging / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D000818:Animals; D015551:Autoimmunity / Q000235:genetics; D005786:Gene Expression Regulation / Q000276:immunology*; D006801:Humans; D008213:Lymphocyte Activation; D053858:Metabolic Networks and Pathways / Q000235:genetics / Q000276:immunology*; D010084:Oxidation-Reduction; D010641:Phenotype; D015398:Signal Transduction; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000473:pathology
keywords: Aging; Free radicals; Mitochondria; Protein oxidation; Redox; Thioredoxin; Treg