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Related Concept Videos

Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
Replicative Cell Senescence02:15

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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
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The T and B lymphocytes of the adaptive immune system develop from common lymphoid progenitor cells in the bone marrow. These progenitors give rise to precursors that eventually develop into both T and B lymphocytes. As these precursors mature, they gain the ability to detect and respond to foreign antigens in the body, a process known as immunocompetence. Additionally, these precursors acquire self-tolerance, a process that ensures they do not react to self-antigens. This intricate system...
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Related Experiment Video

Updated: May 30, 2026

Generation of Induced Regulatory T Cells from Primary Human Naïve and Memory T Cells
14:23

Generation of Induced Regulatory T Cells from Primary Human Naïve and Memory T Cells

Published on: April 16, 2012

Reversible senescence in human CD4+CD45RA+CD27- memory T cells.

Diletta Di Mitri1, Rita I Azevedo, Sian M Henson

  • 1Division of Infection and Immunity, University College London, London W1T 4JF, United Kingdom.

Journal of Immunology (Baltimore, Md. : 1950)
|July 27, 2011
PubMed
Summary

Persistent infections cause T cell senescence. The p38 MAPK pathway actively inhibits telomerase in CD4(+) EMRA T cells, driving senescence, but this process is reversible, offering potential therapeutic targets.

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Published on: August 12, 2018

Area of Science:

  • Immunology
  • Cellular senescence
  • T cell biology

Background:

  • Persistent infections and inflammation lead to T cell terminal differentiation and senescence.
  • The mechanisms regulating end-stage T cell differentiation, particularly in CD4(+) effector memory (EM) and EMRA T cells, remain unclear.
  • CD4(+) EMRA T cells exhibit senescence markers but paradoxically longer telomeres, suggesting active telomerase inhibition.

Purpose of the Study:

  • To investigate the role of the p38 mitogen-activated protein kinase (MAPK) signaling pathway in regulating the senescence of highly differentiated CD4(+) T cells.
  • To determine if p38 MAPK signaling influences telomerase activity and survival in CD4(+) EMRA T cells.

Main Methods:

  • Analysis of CD4(+) T cell subsets (CM, EM, EMRA) for senescence markers (KLRG1, CD57, γH2AX).
  • Measurement of telomere length and telomerase activity.
  • Assessment of p38 MAPK pathway activation (total and phosphorylated p38 expression).
  • Inhibition of p38 MAPK signaling to evaluate effects on telomerase activity and cell survival.

Main Results:

  • CD4(+) EMRA T cells displayed characteristics of terminal differentiation and senescence, including high nuclear γH2AX.
  • Despite defective telomerase activity, CD4(+) EMRA T cells had longer telomeres than other subsets, indicating active inhibition.
  • The p38 MAPK pathway was highly activated in EM and EMRA CD4(+) T cells.
  • Inhibiting p38 MAPK signaling in CD4(+) EMRA T cells restored telomerase activity and improved survival after T cell receptor activation.

Conclusions:

  • Activation of the p38 MAPK pathway contributes to senescence characteristics in highly differentiated CD4(+) T cells.
  • CD4(+) EMRA T cells exhibit telomere-independent senescence regulated by reversible signaling pathways.
  • Targeting the p38 MAPK pathway may offer a strategy to reverse T cell senescence in chronic inflammatory conditions.