Does metabolic reprogramming underpin age-associated changes in T cell phenotype and function?

Rita C. Torrão; Stuart J. Bennett; James E. Brown; Helen R. Griffiths

doi:10.1016/j.freeradbiomed.2014.03.002

Does metabolic reprogramming underpin age-associated changes in T cell phenotype and function?

Rita C. Torrão, Stuart J. Bennett, James E. Brown, Helen R. Griffiths^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

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. © 2014 Elsevier Inc.

Original language	English
Pages (from-to)	26–35
Number of pages	10
Journal	Free Radical Biology and Medicine
Volume	71
Early online date	12 Mar 2014
DOIs	https://doi.org/10.1016/j.freeradbiomed.2014.03.002
Publication status	Published - Jun 2014

Bibliographical note

NOTICE: 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

Keywords

ageing
free radicals
mitochondria
protein oxidation
Redox
thioredoxin
Treg

Access to Document

10.1016/j.freeradbiomed.2014.03.002

Metabolic reprogramming underpin age-associated changes in T cell phenotype and function
NOTICE: 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
Accepted author manuscript, 799 KB

Cite this

@article{e3a9877328dd4d7abfcf905e0d43f91f,

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 na{\"i}ve 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. {\textcopyright} 2014 Elsevier Inc.",

keywords = "ageing, free radicals, mitochondria, protein oxidation, Redox, thioredoxin, Treg",

author = "Torr{\~a}o, {Rita C.} and Bennett, {Stuart J.} and Brown, {James E.} and Griffiths, {Helen R.}",

note = "NOTICE: this is the author{\textquoteright}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 Torr{\~a}o, 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",

year = "2014",

month = jun,

doi = "10.1016/j.freeradbiomed.2014.03.002",

language = "English",

volume = "71",

pages = "26–35",

journal = "Free Radical Biology and Medicine",