Aging and Immune Function: Molecular Mechanisms to Interventions
Open accessAbstract
Abstract The immune system of an organism is an essential component of the defense mechanism aimed at combating pathogenic stress. Age-associated immune dysfunction, also dubbed "immune senescence," manifests as increased susceptibility to infections, increased onset and progression of autoimmune diseases, and onset of neoplasia. Over the years, extensive research has generated consensus in terms of the phenotypic and functional defects within the immune system in various organisms, including humans. Indeed, age-associated alterations such as thymic involution, T cell repertoire skewing, decreased ability to activate naïve T cells and to generate robust memory responses, have been shown to have a causative role in immune decline. Further, understanding the molecular mechanisms underlying the generation of proteotoxic stress, DNA damage response, modulation of ubiquitin proteasome pathway, and regulation of transcription factor NFκB activation, in immune decline, have paved the way to delineating signaling pathways that cross-talk and impact immune senescence. Given the role of the immune system in combating infections, its effectiveness with age may well be a marker of health and a predictor of longevity. It is therefore believed that a better understanding of the mechanisms underlying immune senescence will lead to an effective interventional strategy aimed at improving the health span of individuals. Antioxid. Redox Signal. 14, 1551-1585.
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All possible therapies aimed at non-specifically 'rejuvenating' the immune system might be counterproductive.
“However, all possible therapies aimed at non-specifically “rejuvenating” the immune system might be counterproductive.”
From Immunosenescence and Its Hallmarks: How to Oppose Aging Strategically? A Review of Potential Options for Therapeutic Intervention (2019) · cites this paper as [21]
The different parameters observed between young and older people could also be a product of the adaptation vs. the exposome.
“In fact, the different parameters observed between young and older people could also be a product of the adaption vs. the exposome, i.e., all the stimuli that the immune system has undergone during life.”
From Immunosenescence and Its Hallmarks: How to Oppose Aging Strategically? A Review of Potential Options for Therapeutic Intervention (2019) · cites this paper as [21]
Increased serum levels of TNF-α are also linked to a defective T cell response, in part due to reduced expression of CD28.
“Increased serum levels of TNF-α are also linked to a defective T cell response, in part due to reduced expression of CD28 (21).”
From Immunosenescence and Its Hallmarks: How to Oppose Aging Strategically? A Review of Potential Options for Therapeutic Intervention (2019) · cites this paper as [21]
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Designing the Next Generation of Vaccines: Relevance for Future Pandemics
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Updates on Old and Weary Haematopoiesis
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Down syndrome: is it really characterized by precocious immunosenescence?
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An old problem with new solutions: Strategies to improve vaccine efficacy in the elderly
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- Authors
- Ponnappan, S., & Ponnappan, U.
- Affiliations
- University of Arkansas for Medical Sciences (US)
- Corresponding author
- Ponnappan, Usha
- Venue
- Antioxidants & Redox Signaling
- Publisher
- SAGE Publications
- Published
- 2011-04
- Volume
- 14
- Issue
- 8
- Pages
- 1551-1585
- ISSN
- 1523-0864 (ISSN-L)
- 1557-7716
- PMC
- PMC3061194
- OpenAlex
- W2016256318
- Cited by
- 339
- References
- 419
- Citations by year
- 2026: 8 · 2025: 32 · 2024: 40 · 2023: 28 · 2022: 27 · 2021: 49 · 2020: 25 · 2019: 22 · 2018: 26 · 2017: 26 · 2016: 16 · 2015: 10 · 2014: 7 · 2013: 13 · 2012: 6
- FWCI
- 0.62
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Antioxidants and Redox Signaling (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (AG-13081, AG030599, R01AG013081, AG025220, R01AG030599, R01AG025220)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- immunosenescence, aging, thymic involution, naive T cell activation, memory T cells, proteotoxic stress, DNA damage response, ubiquitin-proteasome system, NF-κB activation, autoimmune disease, cancer susceptibility, healthspan, longevity
- MeSH terms
- Aging, Animals, DNA, Humans, Immune System, T-Lymphocytes, NF-kappa B, Telomere, Reactive Oxygen Species, MicroRNAs
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