Senescent cell clearance by the immune system: Emerging therapeutic opportunities
Open accessAbstract
Senescent cells (SCs) arise from normal cells in multiple organs due to inflammatory, metabolic, DNA damage, or tissue damage signals. SCs are non-proliferating but metabolically active cells that can secrete a range of pro-inflammatory and proteolytic factors as part of the senescence-associated secretory phenotype (SASP). Senescent cell anti-apoptotic pathways (SCAPs) protect SCs from their own pro-apoptotic SASP. SCs can chemo-attract immune cells and are usually cleared by these immune cells. During aging and in multiple chronic diseases, SCs can accumulate in dysfunctional tissues. SCs can impede innate and adaptive immune responses. Whether immune system loss of capacity to clear SCs promotes immune system dysfunction, or conversely whether immune dysfunction permits SC accumulation, are important issues that are not yet fully resolved. SCs may be able to assume distinct states that interact differentially with immune cells, thereby promoting or inhibiting SC clearance, establishing a chronically pro-senescent and pro-inflammatory environment, leading to modulation of the SASP by the immune cells recruited and activated by the SASP. Therapies that enhance immune cell-mediated clearance of SCs could provide a lever for reducing SC burden. Such therapies could include vaccines, small molecule immunomodulators, or other approaches. Senolytics, drugs that selectively eliminate SCs by transiently disabling their SCAPs, may prove to alleviate immune dysfunction in older individuals and thereby accelerate immune-mediated clearance of SCs. The more that can be understood about the interplay between SCs and the immune system, the faster new interventions may be developed to delay, prevent, or treat age-related dysfunction and the multiple senescence-associated chronic diseases and disorders.
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Senescent cells are normally cleared within days to weeks by natural killer cells and other immune cells.
“Normally, senescent cells appear to be cleared within days to weeks after they develop by natural killer cells and other immune cell types62,66–69.”
From Cellular senescence and senolytics: the path to the clinic (2022) · cites this paper as [62]
The Introduction says senescent cells appear to be usually cleared by the immune system, and the NKs section describes natural killer cells clearing senescent-like cells in a liver-fibrosis model, with fibrosis resolving within 20 days. That example does not establish that senescent cells generally are cleared within days to weeks after developing; the Heterogeneous SC hypothesis section also notes that some persist for years. Page numbers are unavailable in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredIn 30-70% of senescent cells, the SASP contains pro-inflammatory, proapoptotic, and pro-fibrotic factors, some of which can make previously non-senescent cells senescent locally and at a distance through endocrine action.
“In 30–70% of senescent cells, this SASP entails pro-inflammatory, proapoptotic and pro-fibrotic factors7,31,40,59–64, some of which can cause previously non-senescent cells to become senescent both locally and at a distance in an endocrine manner24,39,47.”
From Cellular senescence and senolytics: the path to the clinic (2022) · cites this paper as [62]
The SASP section says senescent cells can affect nearby and distant cells through the SASP, including by spreading senescence, and describes inflammatory SASP factors. It does not give the 30–70% figure or characterize the factors as proapoptotic and pro-fibrotic. Although it mentions effects on endocrine function, it does not specify endocrine action as the mechanism by which senescence spreads at a distance. (LLM, conf=0.86)
Experimental — accuracy not yet measuredTransient senescent cells can have beneficial functions: their SASPs can orchestrate tissue remodeling, induce immune responses during infection or injury, promote parturition via placental senescent cells, and attract immune cells to clear pro-inflammatory senescent cells.
“If senescent cells are present transiently, beneficial functions of both the proapoptotic and pro-growth types of SASP can orchestrate tissue remodeling”
From Cellular senescence and senolytics: the path to the clinic (2022) · cites this paper as [62]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredOnce the senescent cell burden passes a threshold, further increases in proapoptotic/pro-inflammatory senescent cells may cause tissue destruction, disease progression, immune dysregulation, and a feed-forward loop of accumulation.
“Once senescent cell burden surpasses this threshold, continuing increases in proapoptotic/pro-inflammatory senescent cell burden may contribute to tissue destruction and hence development or progression of multiple diseases and age-related disorders (Table 2) as well as immune dysregulation, further amplifying senescent cell accumulation in a feed-forward loop36,38,62.”
From Cellular senescence and senolytics: the path to the clinic (2022) · cites this paper as [62]
If a threshold burden of senescent cells is exceeded, they can accumulate, possibly because proapoptotic SASP cells spread senescence by paracrine and endocrine mechanisms faster than immune clearance.
“However, if a threshold burden of senescent cells is exceeded, senescent cells can accumulate, perhaps because proapoptotic SASP-expressing senescent cells induce paracrine and endocrine spread of senescence at a rate exceeding immune clearance of preexisting and newly formed senescent cells24,62”
From Cellular senescence and senolytics: the path to the clinic (2022) · cites this paper as [62]
Modulating immune clearance of senescent cells is another strategy for reducing age-related senescent cell burden and pathologic conditions.
“Other strategies for decreasing age-related senescent cell burden and pathologic conditions involve modulating immune clearance of senescent cells62.”
From Cellular senescence and senolytics: the path to the clinic (2022) · cites this paper as [62]
At younger ages, senescent cells are cleared by the host immune system.
“At younger ages, senescent cells are cleared by the host immune system [63–66]”
From Reducing Senescent Cell Burden in Aging and Disease (2020) · cites this paper as [65]
SASP factors exert tumor suppression activity by promoting recruitment and instruction of immune cells that contribute to elimination of damaged cells.
“SASP factors also exert a tumor suppression activity by promoting the recruitment and instruction of immune cells that contribute to the elimination of damaged cells [290].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [290]
Impaired innate and adaptive immune responses by senescent cells result in persistent accumulation of various senescent cells.
“Immunaging or impaired innate and adaptive immune responses by senescent cells result in persistent accumulation of various senescent cells.”
From Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases (2020) · cites this paper as [122]
Immune cells can remove senescent cells.
“Immune cells can remove senescent cells.”
From Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases (2020) · cites this paper as [122]
Generally, senescent cells can be removed by apoptosis and the immune system.
“Generally, senescent cells can be removed by apoptosis and the immune system [121,122].”
From Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases (2020) · cites this paper as [122]
Senescent cells recruit and make immune cells senescent and dysfunctional via SASP, leading to persistent and excessive accumulation of senescent cells.
“Senescent cells recruit and make immune cells senescent and dysfunctional via SASP, leading to persistent and excessive accumulation of senescent cells [122].”
From Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases (2020) · cites this paper as [122]
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- Authors
- Prata, L. G. P. L., Ovsyannikova, I. G., Tchkonia, T., & Kirkland, J. L.
- Affiliations
- Mayo Clinic (US)
- Corresponding author
- Kirkland, James L.
- Venue
- Seminars in Immunology
- Publisher
- Elsevier BV
- Published
- 2018-12
- Volume
- 40
- Pages
- 101275
- ISSN
- 1044-5323 (ISSN-L)
- PMC
- PMC7061456
- OpenAlex
- W2944421558
- Semantic Scholar
- cf3d214f9e5c32c6028bf094e691da56482a8c89
- Cited by
- 497
- References
- 233
- Citations by year
- 2026: 58 · 2025: 82 · 2024: 73 · 2023: 79 · 2022: 73 · 2021: 77 · 2020: 50 · 2019: 5
- FWCI
- 4.33
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Seminars in Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (AG13925)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Keywords
- senescent cells, senolytics, senescence-associated secretory phenotype, immune dysfunction, aging, immunomodulators, senescence-associated inflammation
- MeSH terms
- Aging, Chronic Disease, Humans, Immune System, Phenotype, Cellular Senescence, Apoptosis
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