Kleemeier Award Lecture 2008 – the canary in the coal mine: telomeres and human healthspan

Effros, R. B.

doi:10.1093/gerona/glp001

Cited by 58Telomeres, Telomerase, and SenescenceGenetics, Aging, and Longevity in Model OrganismsT-cell and B-cell Immunology

Kleemeier Award Lecture 2008 – the canary in the coal mine: telomeres and human healthspan

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Effros, R. B.·2009·The Journals of Gerontology Series A: Biological Sciences and Medical Sciences

DOI 10.1093/gerona/glp001PMC PMC2800806

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Abstract

Telomeres, the repeated series of DNA sequences that cap the ends of linear chromosomes, become shorter during cell division and oxidative stress. Shortened telomeres have been documented in a wide variety of pathologies associated with aging and are also predictive of early mortality in the very old. However, telomere shortening--like the canary in the coal mine--is not the cause of the deleterious effects, but rather, the harbinger of increased health risk. Using immune responses to infection as a model system to further analyze the link between telomeres and age-related disease, we have demonstrated that the end-stage T cell with shortened telomeres is reduced in antiviral immune function and secretes large amounts of so-called proinflammatory factors. Our research has documented that maintaining high levels of the telomere-extending enzyme, telomerase, by either genetic manipulation or exposure of T cells to chemical telomerase activators, not only retards telomere loss but also restores a more youthful functional profile to the T cells. These observations suggest possible novel telomerase-based therapeutic approaches to enhancing healthspan in the elderly population.

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Immune cells that have become senescent due to critical telomere shortening hyper-secrete pro-inflammatory cytokines such as IL-6 and TNF-α, which can lead to a vicious cycle of further inflammation, oxidative stress and telomere shortening.
“In addition, immune cells that have become senescent due to critical telomere shortening (e.g., CD8+CD28− T lymphocytes) hyper-secrete pro-inflammatory cytokines such as interleukin (IL)-6 and tumor necrosis factor (TNF)-α (Effros, 2009), which can lead to a vicious cycle of further inflammation, oxidative stress and telomere shortening.”
From Psychiatric disorders and leukocyte telomere length: Underlying mechanisms linking mental illness with cellular aging (2015) · cites this paper as Effros, 2009

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Authors: Effros, R. B.
Affiliations: University of California, Los Angeles (US)
Corresponding author: Effros, R. B.
ORCID: Effros, R. B.
Venue: The Journals of Gerontology Series A: Biological Sciences and Medical Sciences
Publisher: Oxford University Press (OUP)
Published: 2009-02-19
Volume: 64A
Issue: 5
Pages: 511-515
ISSN: 1079-5006 (ISSN-L)
1758-535X
DOI: 10.1093/gerona/glp001
PMC: PMC2800806
OpenAlex: W2107938016
Cited by: 58
References: 35
Citations by year: 2025: 2 · 2024: 2 · 2023: 1 · 2022: 3 · 2021: 1 · 2020: 3 · 2019: 5 · 2018: 4 · 2017: 4 · 2016: 4 · 2015: 3 · 2014: 3 · 2013: 3 · 2012: 5
FWCI: 0.73
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: The Journals of Gerontology Series A (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
HighWire Press Open Archive (submittedVersion)
Funders: U.S. Public Health Service
National Institute on Aging (R01AG023720, AG 023720)
National Institute of Allergy and Infectious Diseases (R01AI060362, AI028697, AI 060362, P30AI028697)
Topics: Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords: telomeres, healthspan, aging, telomere shortening, telomerase, T cells, inflammatory cytokines, age-related diseases, telomerase activators, oxidative stress
MeSH terms: Aging, Cell Division, Humans, T-Lymphocytes, Telomere

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