Next steps in mechanisms of inflammaging

Leena P. Bharath, Barbara S. Nikolajczyk

Research output: Contribution to journalComment/debate

3 Scopus citations

Abstract

Striking age-related changes occur in the human immune system, beginning in the sixth decade of life. Age is a non-modifiable, universal risk factor that results in the dysregulation of many cellular homeostatic processes. The decline in immune cell macroautophagy/autophagy and the increased generation of proinflammatory cytokines during agingfuels the development of diseases in the elderly. We reported that higher Th17 inflammation during aging was secondary to dysregulation in T cell autophagy. However, the mechanism underlying lower anti-CD3 and anti-CD28 activation-induced T cell autophagy during aging remain unknown. Our data fuel the speculation that dysregulation of the glutathione (GSH) system might cause the decline in T cell autophagy in aging, additionally provoked by reactive oxygen species signaling emanating from the mitochondria.

Original languageEnglish
Pages (from-to)2285-2286
Number of pages2
JournalAutophagy
Volume16
Issue number12
DOIs
StatePublished - 2020

Bibliographical note

Publisher Copyright:
© 2020 Informa UK Limited, trading as Taylor & Francis Group.

Keywords

  • Aging
  • autophagy
  • glutathione
  • membrane potential
  • mitochondria
  • oxidative stress

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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