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 language | English |
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Pages (from-to) | 2285-2286 |
Number of pages | 2 |
Journal | Autophagy |
Volume | 16 |
Issue number | 12 |
DOIs |
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State | Published - 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