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. © 2014 Elsevier Inc.
|Number of pages||10|
|Journal||Free Radical Biology and Medicine|
|Early online date||12 Mar 2014|
|Publication status||Published - Jun 2014|
Bibliographical noteNOTICE: this is the author’s version of a work that was accepted for publication in Free Radical Biology and Medicine. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Torrão, R. C., Bennett, S. J., Brown, J. E., & Griffiths, H. R. Does metabolic reprogramming underpin age-associated changes in T cell phenotype and function?. Free radical biology and medicine, 71, 26–35. (2014) DOI http://dx.doi.org/10.1016/j.freeradbiomed.2014.03.002
- free radicals
- protein oxidation