Cited by 116Autophagy in Disease and TherapyT-cell and B-cell ImmunologyMitochondrial Function and Pathology

Age-associated changes in human CD4+ T cells point to mitochondrial dysfunction consequent to impaired autophagy

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Bektas, Arsun, Schurman, Shepherd H., Gonzalez-Freire, Marta, Dunn, Christopher A., Singh, Amit K., Macian, Fernando, Cuervo, Ana Maria, Sen, Ranjan +1 more·2019·Aging

Abstract

T lymphocytes caused by defective mitochondrial turnover by autophagy, which may trigger chronic inflammation and contribute to the impairment of immune defense in older persons.

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Crossref · 10.18632/aging.102438

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  • Aging is associated with alterations in mitochondrial function and mitochondrial dynamics in memory T cells.

    “The changes in the adaptive immune system, namely T-cells, with aging has been reported; memory T-cell function substantially decreases with aging (8,9), with alterations in mitochondrial function and mitochondrial dynamics (8–10).”

    From Alzheimer's Disease–Associated Amyloid-β Precursor Protein Prevents Aging Stress–Induced Mitophagy and Fumarate Depletion to Improve Antitumor Immunity (2025) · cites this paper as [10]

    The Results section on mitochondrial morphology reports dysmorphic mitochondria and undegraded autophagic compartments in older participants’ memory CD4+ T cells, supporting an age-related alteration in mitochondrial turnover. The respiration Results find reduced mitochondrial function in older participants’ CD4+ T cells overall, but do not establish that reduction specifically in memory T cells. (LLM, conf=0.84)

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Research works printed but not linked: 2

  1. [2]Council NR. 6, Environmental Effects on Age-Associated Diseases and Changes in Organ Function. Aging. Today’s Environment. Washington (DC): The National Academies Press; 1987.
  2. [52]Gnaiger E, Renner-Sattler KK. High-resolution respirometry and coupling control protocol with intact cells: ROUTINE, LEAK, ETS, ROX. Mitochondrial Physiology Network. 2014; 08: 1– 8.

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Authors
Bektas, A., Schurman, S. H., Gonzalez-Freire, M., Dunn, C. A., Singh, A. K., Macian, F., Cuervo, A. M., Sen, R., & Ferrucci, L.
Affiliations
  • National Institutes of Health (US)
  • Translational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
  • Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
  • Institute for Aging Studies, Albert Einstein College of Medicine, Bronx, NY 10461, USA
Corresponding author
Ferrucci, Luigi
Venue
Aging
Published
2019-11-09
Volume
11
Issue
21
Pages
9234-9263
ISSN
1945-4589 (ISSN-L)
OpenAlex
W2982745597
Cited by
116
References
54
Citations by year
2026: 14 · 2025: 25 · 2024: 14 · 2023: 24 · 2022: 11 · 2021: 16 · 2020: 12
FWCI
7.42
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Aging (publishedVersion)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
  • Johns Hopkins University
  • National Institutes of Health (AG038072)
  • National Institute on Aging (P01AG031782, P30AG038072, AG038072)
  • National Heart, Lung, and Blood Institute
  • National Institute of Environmental Health Sciences
Topics
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords
CD4+ T cells, mitochondrial dysfunction, autophagy, mitochondrial turnover, chronic inflammation, immunosenescence, T lymphocyte function
MeSH terms
Immunosenescence, Adult, Aged, Humans, Longitudinal Studies, Mitochondria, CD4-Positive T-Lymphocytes, Cell Respiration, Young Adult, Mitophagy

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