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Deciphering the impact of TERT/telomerase on immunosenescence and T cell revitalization


Review

. 2024 Sep 23:15:1465006.


doi: 10.3389/fimmu.2024.1465006.


eCollection 2024.

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Review

Lingyi Huang et al.


Front Immunol.


.

Abstract

Immunosenescence impacts both the innate and adaptive immune systems, predominantly affecting certain immune cell types. A notable manifestation of immunosenescence is the diminished efficacy of adaptive immunity. The excessive senescence of immune cells, particularly T cells, leads to marked immune deficiency, consequently escalating the risk of infections, tumors, and age-associated disorders. Lymphocytes, especially T cells, are subject to both replicative and premature senescence. Telomerase reverse transcriptase (TERT) and telomerase have multifaceted roles in regulating cellular behavior, possessing the ability to counteract both replicative and premature senescence in lymphocytes. This review encapsulates recent advancements in understanding immunosenescence, with a focus on T cell senescence, and the regulatory mechanisms involving TERT/telomerase. Additionally, it comprehensively discusses strategies aimed at inhibiting immunosenescence by augmenting TERT/telomerase activity.


Keywords:

CD28; T lymphocytes; immunosenescence; telomerase; telomerase reverse transcriptase (TERT).

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures


Figure 1



Figure 1

Primary Mechanism of TERT/Telomerase Regulation in T Cell Immunosenescence. Some factors such as TNFα, PGE2 and IFN-α released by senescent, activated or infected non-immune somatic cells or immune cells down-regulate CD28 protein expression, attenuate TERT expression and telomerase activation in T cells, thereby weakening the resistance of TERT and telomerase to premature and replicative senescence of T cells, resulting in reduce of effector T cells, increase of memory T cells, and enhancement of inflammaging.

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Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This work was supported by the National Natural Science Foundation of China (82371717); the Grant from the Science and Technology Bureau of Sichuan Province (2024NSFSC0047).


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