The DOI matches its Crossref record; 96 of the 96 references it cites were found in a registry or an index.
Are senescence and exhaustion intertwined or unrelated processes that compromise immunity?
Abstract
Can the immune system be reactivated continuously throughout the lifetime of an organism or is there a finite point at which repeated antigenic challenge leads to the loss of lymphocyte function or the cells themselves or both? Replicative senescence and exhaustion are processes that control T cell proliferative activity and function; however, there is considerable confusion over the relationship between these two intrinsic cellular control mechanisms. In this Opinion article, we compare the molecular regulation of senescence and exhaustion in T cells. Available data suggest that both processes are regulated independently of each other and that it may be safer to block exhaustion than senescence to enhance immunity.
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In the citing paper
“In addition to phenotypic alteration, senescent T cells manifest defective killing abilities and the development of negative regulatory functions [52,53].”
From T cell anergy, exhaustion, senescence, and stemness in the tumor microenvironment (2013) · cites this paper as [53]
In the citing paper
“Based on phenotype and function, senescent T cells must not be confused with exhausted T cells induced by prolonged antigen stimulation [40–42].”
From T-cell aging in rheumatoid arthritis (2014) · cites this paper as [42]
In the citing paper
“The restriction to the extent of proliferation of T cells, especially those that are specific for frequently encountered or persistent antigens may therefore compromise the maintenance of specific immunity in older humans as they may be driven towards senescence [1, 12].”
From Senescence of T Lymphocytes: Implications for Enhancing Human Immunity (2016) · cites this paper as [12]
In the citing paper
“Short telomeres are interpreted as DNA damage by cell sensing machinery that initiates a cascade of events that culminates in growth arrest (reviewed in Akbar and Henson 2011 [12]).”
From Senescence of T Lymphocytes: Implications for Enhancing Human Immunity (2016) · cites this paper as [12]
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Metadata
- Authors
- Akbar, A. N., & Henson, S. M.
- Affiliations
- University College London (GB)
- Corresponding author
- Akbar, Arne N.
- ORCID
- Akbar, Arne N.
- Venue
- Nature Reviews Immunology
- Published
- 2011-03-25
- Volume
- 11
- Issue
- 4
- Pages
- 289-295
- ISSN
- 1474-1733 (ISSN-L)
- 1474-1741
- OpenAlex
- W2068367301
- Cited by
- 474
- References
- 96
- Citations by year
- 2026: 36 · 2025: 41 · 2024: 28 · 2023: 28 · 2022: 38 · 2021: 36 · 2020: 33 · 2019: 32 · 2018: 31 · 2017: 20 · 2016: 33 · 2015: 32 · 2014: 26 · 2013: 29 · 2012: 20
- FWCI
- 2.43
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nature reviews. Immunology (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- Wellcome Trust
- Biotechnology and Biological Sciences Research Council
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Keywords
- T cell senescence, T cell exhaustion, replicative senescence, viral persistence, aging, immune reactivation, T cell proliferation, immunosenescence
- MeSH terms
- Animals, Fatigue, Humans, Immunity, Cellular, Lymphocyte Activation, T-Lymphocytes, Virus Diseases, Cellular Senescence, Mice
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