Cited by 442T-cell and B-cell ImmunologyTelomeres, Telomerase, and SenescenceGenetics, Aging, and Longevity in Model Organisms

Contributions of Age-Related Thymic Involution to Immunosenescence and Inflammaging

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Thomas, Rachel, Wang, Weikan, Su, Dong-Ming·2020·Immunity & Ageing

Abstract

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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Research works printed but not linked: 5

  1. [3]Pawelec G Immunosenescence comes of age. Symposium on Aging Research in Immunology: The Impact of Genomics EMBO Rep 2007 8 3 220 223 10.1038/sj.embor.7400922 17304236 PMC1808042 · DOI
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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)
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
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

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