Contributions of Age-Related Thymic Involution to Immunosenescence and Inflammaging
Open accessAbstract
Immune system aging is characterized by the paradox of immunosenescence (insufficiency) and inflammaging (over-reaction), which incorporate two sides of the same coin, resulting in immune disorder. Immunosenescence refers to disruption in the structural architecture of immune organs and dysfunction in immune responses, resulting from both aged innate and adaptive immunity. Inflammaging, described as a chronic, sterile, systemic inflammatory condition associated with advanced age, is mainly attributed to somatic cellular senescence-associated secretory phenotype (SASP) and age-related autoimmune predisposition. However, the inability to reduce senescent somatic cells (SSCs), because of immunosenescence, exacerbates inflammaging. Age-related adaptive immune system deviations, particularly altered T cell function, are derived from age-related thymic atrophy or involution, a hallmark of thymic aging. Recently, there have been major developments in understanding how age-related thymic involution contributes to inflammaging and immunosenescence at the cellular and molecular levels, including genetic and epigenetic regulation, as well as developments of many potential rejuvenation strategies. Herein, we discuss the research progress uncovering how age-related thymic involution contributes to immunosenescence and inflammaging, as well as their intersection. We also describe how T cell adaptive immunity mediates inflammaging and plays a crucial role in the progression of age-related neurological and cardiovascular diseases, as well as cancer. We then briefly outline the underlying cellular and molecular mechanisms of age-related thymic involution, and finally summarize potential rejuvenation strategies to restore aged thymic function.
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Production of senescence-associated secretory phenotype (SASP) is an important feature of immunosenescence.
“T cell–output decline is an important feature of immunosenescence as well as the production of senescence-associated secretory phenotype, increased glycolysis, and reactive oxygen species.”
From Immunosenescence: a key player in cancer development (2020) · cites this paper as [25]
T cell output decline is an important feature of immunosenescence.
“T cell–output decline is an important feature of immunosenescence as well as the production of senescence-associated secretory phenotype, increased glycolysis, and reactive oxygen species.”
From Immunosenescence: a key player in cancer development (2020) · cites this paper as [25]
Thymus degeneration leads to a decrease in the number and proportion of CD8+ naïve T cells, which is one of the main manifestations of immunosenescence.
“Thymus degeneration leads to a decrease in the number and proportion of CD8+ naïve T cells, which is one of the main manifestations of immunosenescence [24, 25] (Fig. 2).”
From Immunosenescence: a key player in cancer development (2020) · cites this paper as [25]
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- Authors
- Thomas, R., Wang, W., & Su, D.-M.
- Affiliations
- University of North Texas Health Science Center (US)
- Corresponding author
- Su, Dong-Ming
- Venue
- Immunity & Ageing
- Published
- 2020-01-20
- Volume
- 17
- Issue
- 1
- Pages
- 2-2
- ISSN
- 1742-4933 (ISSN-L)
- PMC
- PMC6971920
- OpenAlex
- W3010019019
- Cited by
- 442
- References
- 249
- Citations by year
- 2026: 69 · 2025: 76 · 2024: 84 · 2023: 64 · 2022: 51 · 2021: 58 · 2020: 40
- FWCI
- 5.39
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Immunity & Ageing (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (R01AI121147)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- thymic involution, immunosenescence, inflammaging, thymic aging, T cell function, cellular senescence, senescence-associated secretory phenotype, epigenetic regulation, age-related neurological diseases, age-related cardiovascular disease
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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