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

Rita C Torrão1, Stuart J Bennett1, James E Brown1

  • 1Life and Health Sciences and Aston Research Centre for Healthy Ageing, Aston University, Birmingham B4 7ET, West Midlands, UK.

Free Radical Biology & Medicine
|March 18, 2014
PubMed
Summary
This summary is machine-generated.

Aging impairs T cell function, leading to weaker immunity and increased autoimmunity. This decline is linked to changes in T cell populations, redox balance, and metabolism.

Keywords:
AgingFree radicalsMitochondriaProtein oxidationRedoxThioredoxinTreg

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Area of Science:

  • Immunology
  • Gerontology
  • Cellular Metabolism

Background:

  • Adaptive immunity relies on T cells to identify and eliminate foreign material.
  • Aging is associated with diminished T cell function, impacting infection response, vaccination efficacy, and autoimmunity.
  • Key age-related changes include reduced naive CD4(+) T cells, increased antigen-experienced CD4(+) T cells, loss of redox homeostasis, and impaired metabolic switching.

Purpose of the Study:

  • To explore how metabolic programming and loss of redox homeostasis contribute to age-associated changes in T cell phenotype and function.

Main Methods:

  • This article reviews existing literature and research on T cell function, aging, metabolism, and redox homeostasis.

Main Results:

  • Aging leads to a decrease in naive T cells and an increase in experienced T cells.
  • Loss of redox homeostasis and impaired metabolic switching are observed in aging T cells.
  • These changes affect T cell phenotype and functional capacity.

Conclusions:

  • Metabolic programming and disrupted redox homeostasis are significant factors in age-related T cell dysfunction.
  • Understanding these mechanisms is crucial for addressing the immunological consequences of aging.