The convergence of senescence and nutrient sensing during lymphocyte ageing
Open accessAbstract
Immunosurveillance requires the migration of lymphocytes and their activation to induce proliferation and effector function. Effective immunity requires an optimal supply of nutrients to lymphocytes. Cells contain nutrient sensing apparatus such as adenosine 5'-monophosphate-activated protein kinase (AMPK) that surveys intracellular ATP levels. Immunity declines during ageing and one possibility is that the energy balance may be altered in old lymphocytes. This paper summarizes recent data identifying a convergence of senescence and nutrient signalling pathways in lymphocytes that inhibit both T cell and natural killer (NK) cell function during ageing. Significantly, these pathways can be inhibited to enhance the activity of these cells.
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Inhibition of nutrient signaling pathways may enhance the activity of lymphocytes from older adults.
“Data suggesting that nutrient signaling pathways may negatively influence lymphocyte function in aging indicate the possibility that inhibition of these pathways may enhance the activity of lymphocytes from older adults (210).”
From Immunosenescence and Its Hallmarks: How to Oppose Aging Strategically? A Review of Potential Options for Therapeutic Intervention (2019) · cites this paper as [210]
Nutrient signaling pathways may negatively influence lymphocyte function in aging.
“Data suggesting that nutrient signaling pathways may negatively influence lymphocyte function in aging indicate the possibility that inhibition of these pathways may enhance the activity of lymphocytes from older adults (210).”
From Immunosenescence and Its Hallmarks: How to Oppose Aging Strategically? A Review of Potential Options for Therapeutic Intervention (2019) · cites this paper as [210]
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- Authors
- Akbar, A. N.
- Affiliations
- University College London (GB)
- Corresponding author
- Akbar, A N
- ORCID
- Akbar, A N
- Venue
- Clinical and Experimental Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2016-10-28
- Volume
- 187
- Issue
- 1
- Pages
- 4-5
- ISSN
- 0009-9104 (ISSN-L)
- 1365-2249
- PMC
- PMC5167018
- OpenAlex
- W2529290665
- Cited by
- 23
- References
- 8
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 2 · 2023: 2 · 2022: 4 · 2021: 4 · 2019: 2 · 2018: 5 · 2016: 1
- FWCI
- 1.44
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Clinical & Experimental Immunology (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- Medical Research Council (MR/M003833/1)
- Biotechnology and Biological Sciences Research Council (BB/G530433/1, BB/J006750/1, BB/E019188/1)
- Topics
- 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
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Keywords
- cellular senescence, nutrient sensing, AMPK, energy metabolism, T cell function, natural killer cells, immunosenescence, immunometabolism
- MeSH terms
- Adenosine Triphosphate, Animals, Energy Metabolism, Humans, Immunologic Surveillance, Killer Cells, Natural, Lymphocyte Activation, T-Lymphocytes, Signal Transduction, Cellular Senescence, AMP-Activated Protein Kinases
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