The DOI matches its Crossref record; 419 of the 419 references it cites were found in a registry or an index.
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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“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]
In the citing paper
“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]
In the citing paper
“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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Flagged first, then by citations
Research works printed but not linked: 2
- 10.1016/j.stem.2007.02.001 · DOI · Paper page
- Ponnappan S, , Ponnappan U. Ubiquitin-proteasome pathway in immune-senescence. Recent Research Developments in Biochemistry Vol. 4 Part II. Pandalai S. Trivandrum, India: Research Signpost, 2003; 779–785.
Cited by
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Immunosenescence: molecular mechanisms and diseases
Liu, Z., Liang, Q., Ren, Y., Guo, C., Ge, X., Wang, L., Cheng, Q., Luo, P., Zhang, Y., & Han, X. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01451-2 · Cited by 1,082
Aiello, A., Farzaneh, F., Candore, G., Caruso, C., Davinelli, S., Gambino, C. M., Ligotti, M. E., Zareian, N., & Accardi, G. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.02247 · Cited by 693
Immunosenescence: a key player in cancer development
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Bajaj, V., Gadi, N., Spihlman, A. P., Wu, S. C., Choi, C. H., & Moulton, V. R. (2021) · Frontiers in Physiology · doi:10.3389/fphys.2020.571416 · Cited by 476
Chung, H. Y., Kim, D. H., Lee, E. K., Chung, K. W., Chung, S., Lee, B., Seo, A. Y., Chung, J. H., Jung, Y. S., Im, E., et al. (2018) · Aging and Disease · doi:10.14336/ad.2018.0324 · Cited by 512
Metadata
- 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
- 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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