Aging of the T Cell Compartment in Mice and Humans: From No Naive Expectations to Foggy Memories
Open accessAbstract
Until the mid-20th century, infectious diseases were the major cause of morbidity and mortality in humans. Massive vaccination campaigns, antibiotics, antivirals, and advanced public health measures drastically reduced sickness and death from infections in children and younger adults. However, older adults (>65 y of age) remain vulnerable to infections, and infectious diseases remain among the top 5–10 causes of death in this population. The aging of the immune system, often referred to as immune senescence, is the key phenomenon underlying this vulnerability. This review centers on age-related changes in T cells, which are dramatically and reproducibly altered with aging. I discuss changes in T cell production, maintenance, function, and response to latent persistent infection, particularly against CMV, which exerts a profound influence on the aging T cell pool, concluding with a brief list of measures to improve immune function in older adults.
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A marked change in aging relates to the composition and functionality of CD4 T cells.
“A marked change observed in aging relates to the composition and functionality of CD4 T cells, the main orchestrators of adaptive immune responses (1–3).”
From Aging promotes reorganization of the CD4 T cell landscape toward extreme regulatory and effector phenotypes (2019) · cites this paper as [2]
The increased turnover of naive CD8+ T cells in later life comes from CD95+CD45RA+CD28+ cells that are reverted memory cells, memory stem cells, or extensively homeostatically proliferated cells resembling murine virtual memory.
“This increased turnover does not derive from truly naive cells, but from CD95+CD45RA+CD28+ T cells that represent reverted memory cells (Pulko et al., 2016), memory stem cells (Fuertes Marraco et al., 2015), or cells that have undergone extensive homeostatic proliferation reminiscent of murine virtual memory cells”
From Successful and Maladaptive T Cell Aging (2017) · cites this paper as Nikolich-Žugich, 2014
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References 105 · Cited by 259
- Authors
- Nikolich-Žugich, J.
- Affiliations
- Department of Immunobiology, University of Arizona College of Medicine , Tucson, AZ 85724
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2014-09
- Volume
- 193
- Issue
- 6
- Pages
- 2622-2629
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC4157314
- OpenAlex
- W1922712900
- Cited by
- 259
- References
- 105
- Citations by year
- 2026: 8 · 2025: 21 · 2024: 12 · 2023: 22 · 2022: 11 · 2021: 31 · 2020: 28 · 2019: 35 · 2018: 27 · 2017: 24 · 2016: 23 · 2015: 16 · 2014: 1
- FWCI
- 2.08
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (n01ai50027-8-0-1)
- U.S. Public Health Service (HHSN272201100017C, HHSN272200900059C)
- National Institute on Aging (AG035309, R01AG035309, R01AG020719, AG020719, R37AG020719)
- National Institute of Allergy and Infectious Diseases (AI81680, U54AI081680, R01AI082529, N01 AI050027)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Keywords
- immunosenescence, T cell senescence, T cell compartment, older adults, infection susceptibility, cytomegalovirus, T cell production, T cell function, age-related immune decline
- MeSH terms
- Aging, Animals, Cell Communication, Cytomegalovirus, Humans, Immunologic Memory, Lymphocyte Activation, CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Mice
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