Cited by 339Genetics, Aging, and Longevity in Model OrganismsTelomeres, Telomerase, and SenescenceT-cell and B-cell Immunology

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Aging and Immune Function: Molecular Mechanisms to Interventions

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Ponnappan, Subramaniam, Ponnappan, Usha·2011·Antioxidants & Redox Signaling

DOI 10.1089/ars.2010.3228PMC PMC3061194

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Abstract

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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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
DOI: 10.1089/ars.2010.3228
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
Licence: journals.sagepub.com/page/policies/text-and-data-mining-license (tdm)
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
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › 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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Aging and Immune Function: Molecular Mechanisms to Interventions

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