Senescent T cells: Beneficial and detrimental roles

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Abstract

<p xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" dir="auto" id="d5487848e277">As the thymus involutes during aging, the T‐cell pool has to be maintained by the periodic expansion of preexisting T cells during adulthood. A conundrum is that repeated episodes of activation and proliferation drive the differentiation of T cells toward replicative senescence, due to telomere erosion. This review discusses mechanisms that regulate the end‐stage differentiation (senescence) of T cells. Although these cells, within both CD4 and CD8 compartments, lose proliferative activity after antigen‐specific challenge, they acquire innate‐like immune function. While this may confer broad immune protection during aging, these senescent T cells may also cause immunopathology, especially in the context of excessive inflammation in tissue microenvironments. </p>

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The senescence-associated secretory phenotype: the dark side of tumor suppression.

Jean-Philippe Coppe, Pierre-Yves Desprez, Ana Krtolica … (2010)

Cellular senescence is a tumor-suppressive mechanism that permanently arrests cells at risk for malignant transformation. However, accumulating evidence shows that senescent cells can have deleterious effects on the tissue microenvironment. The most significant of these effects is the acquisition of a senescence-associated secretory phenotype (SASP) that turns senescent fibroblasts into proinflammatory cells that have the ability to promote tumor progression.

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Chronic inflammation (inflammaging) and its potential contribution to age-associated diseases.

Claudio Franceschi, Judith Campisi (2014)

Human aging is characterized by a chronic, low-grade inflammation, and this phenomenon has been termed as "inflammaging." Inflammaging is a highly significant risk factor for both morbidity and mortality in the elderly people, as most if not all age-related diseases share an inflammatory pathogenesis. Nevertheless, the precise etiology of inflammaging and its potential causal role in contributing to adverse health outcomes remain largely unknown. The identification of pathways that control age-related inflammation across multiple systems is therefore important in order to understand whether treatments that modulate inflammaging may be beneficial in old people. The session on inflammation of the Advances in Gerosciences meeting held at the National Institutes of Health/National Institute on Aging in Bethesda on October 30 and 31, 2013 was aimed at defining these important unanswered questions about inflammaging. This article reports the main outcomes of this session. © The Author 2014. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

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Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders.

Darren J. Baker, Tobias Wijshake, Tamar Tchkonia … (2012)

Advanced age is the main risk factor for most chronic diseases and functional deficits in humans, but the fundamental mechanisms that drive ageing remain largely unknown, impeding the development of interventions that might delay or prevent age-related disorders and maximize healthy lifespan. Cellular senescence, which halts the proliferation of damaged or dysfunctional cells, is an important mechanism to constrain the malignant progression of tumour cells. Senescent cells accumulate in various tissues and organs with ageing and have been hypothesized to disrupt tissue structure and function because of the components they secrete. However, whether senescent cells are causally implicated in age-related dysfunction and whether their removal is beneficial has remained unknown. To address these fundamental questions, we made use of a biomarker for senescence, p16(Ink4a), to design a novel transgene, INK-ATTAC, for inducible elimination of p16(Ink4a)-positive senescent cells upon administration of a drug. Here we show that in the BubR1 progeroid mouse background, INK-ATTAC removes p16(Ink4a)-positive senescent cells upon drug treatment. In tissues--such as adipose tissue, skeletal muscle and eye--in which p16(Ink4a) contributes to the acquisition of age-related pathologies, life-long removal of p16(Ink4a)-expressing cells delayed onset of these phenotypes. Furthermore, late-life clearance attenuated progression of already established age-related disorders. These data indicate that cellular senescence is causally implicated in generating age-related phenotypes and that removal of senescent cells can prevent or delay tissue dysfunction and extend healthspan.

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Phatthamon Laphanuwat: (View ORCID Profile)

Journal

Title: Immunological Reviews

Abbreviated Title: Immunological Reviews

Publisher: Wiley

ISSN (Print): 0105-2896

ISSN (Electronic): 1600-065X

Publication date (Electronic): April 25 2023

Affiliations

[1 ]Division of Medicine University College London London UK

[2 ]Núcleo de Doenças Infecciosas Universidade Federal do Espírito Santo Vitoria Brazil

[3 ]Núcleo de Biotecnologia Universidade Federal do Espírito Santo Vitoria Brazil

Article

DOI: 10.1111/imr.13206

SO-VID: 62681cb1-7619-43b7-a3c3-628b8e6844bf

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http://creativecommons.org/licenses/by/4.0/

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Senescent T cells: Beneficial and detrimental roles

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UCL: UN SDG 03 Good Health and Well-Being

Most cited references 191

The senescence-associated secretory phenotype: the dark side of tumor suppression.

Chronic inflammation (inflammaging) and its potential contribution to age-associated diseases.

Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders.

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