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Telomeres and immunological diseases of aging.
Open accessAbstract
A defining feature of the eukaryotic genome is the presence of linear chromosomes. This arrangement, however, poses several challenges with regard to chromosomal replication and maintenance. To prevent the loss of coding sequences and to suppress gross chromosomal rearrangements, linear chromosomes are capped by repetitive nucleoprotein structures, called telomeres. Each cell division results in a progressive shortening of telomeres that, below a certain threshold, promotes genome instability, senescence, and apoptosis. Telomeric erosion, maintenance, and repair take center stage in determining cell fate. Cells of the immune system are under enormous proliferative demand, stressing telomeric intactness. Lymphocytes are capable of upregulating telomerase, an enzyme that can elongate telomeric sequences and, thus, prolong cellular lifespan. Therefore, telomere dynamics are critical in preserving immune function and have become a focus for studies of immunosenescence and autoimmunity. In this review, we describe the role of telomeric nucleoproteins in shaping telomere architecture and in suppressing DNA damage responses. We summarize new insights into the regulation of telomerase activity, hereditary disorders associated with telomere dysfunction, the role of telomere loss in immune aging, and the impact of telomere dysfunction in chronic inflammatory disease.
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“In contrast to most other somatic cells, they have the ability to reactivate telomerase, elongate telomeres and thus lengthen their life span [13].”
From T-cell aging in rheumatoid arthritis (2014) · cites this paper as [13]
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“HIV-associated inflammation and/or exposure to nucleoside analogues have been associated with changes in these and other key biologic pathways (33–40).”
From HIV and Aging: State of Knowledge and Areas of Critical Need for Research. A Report to the NIH Office of AIDS Research by the HIV and Aging Working Group (2012) · cites this paper as [37]
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Metadata
- Authors
- Andrews, N. P., Fujii, H., Goronzy, J. J., & Weyand, C. M.
- Affiliations
- Emory University (US)
- Venue
- Gerontology
- Publisher
- S. Karger AG
- Published
- 2009-12-17
- Volume
- 56
- Issue
- 4
- Pages
- 390-403
- ISSN
- 0304-324X (ISSN-L)
- 1423-0003
- PMC
- PMC2917738
- OpenAlex
- W1981392889
- Cited by
- 108
- References
- 148
- Citations by year
- 2025: 3 · 2024: 12 · 2023: 4 · 2022: 5 · 2021: 5 · 2020: 5 · 2019: 5 · 2018: 9 · 2017: 2 · 2016: 5 · 2015: 7 · 2014: 12 · 2013: 8 · 2012: 15
- FWCI
- 0.91
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Gerontology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American College of Rheumatology Research and Education Foundation
- Rheumatology Research Foundation
- National Institutes of Health
- National Institute on Aging (R01AG015043, R01AG15043)
- National Heart, Lung, and Blood Institute (R01HL117913)
- National Eye Institute (R01EY011916, R01 EY 11916)
- National Institute of Allergy and Infectious Diseases (R01AI044142, U19-AI57266, R01AI44142, R01AI108906, R56AI044142, U19AI057266)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR041974, R01 AR 41974, R01AR042527, R01AR42527)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
- Keywords
- telomeres, immunosenescence, autoimmunity, telomerase, telomere dysfunction, lymphocytes, telomere maintenance, DNA damage response, chronic inflammatory diseases, genomic instability, cellular senescence, apoptosis
- MeSH terms
- Aging, Animals, Humans, Immune System Diseases, Inflammation, Models, Biological, T-Lymphocytes, Gene Expression Regulation, Enzymologic, Telomere, Cellular Senescence, Telomerase, Aging, Premature
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