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CD4 T cells acquire Eomesodermin to modulate cellular senescence and aging.

Yehezqel Elyahu1,2,3, Ilana Feygin1,2, Ekaterina Eremenko1,2

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Aging causes tissue decline, but immune cells called CD4 T lymphocytes (CD4-Eomes) help manage senescent cells. Eliminating these cells accelerates aging and disease, highlighting their role in longevity.

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Area of Science:

  • Immunology
  • Gerontology
  • Cellular Biology

Background:

  • Aging leads to tissue dysfunction and increased disease susceptibility.
  • Senescent cells (SCs) accumulate with age, but their immune regulation is poorly understood.
  • CD4 T cells are key immune players, but their role in managing senescence is unclear.

Purpose of the Study:

  • To investigate the role of CD4 T lymphocytes in regulating senescent cell burden during aging.
  • To determine the impact of CD4-Eomes cells on age-related tissue deterioration and lifespan.
  • To explore the function of CD4-Eomes cells in chronic inflammatory conditions like liver cirrhosis.

Main Methods:

  • Observation of CD4 T cell differentiation into Eomesodermin (Eomes)+CCL5+ T lymphocytes (CD4-Eomes) in SC-rich environments.
  • Utilizing senolytic drugs to reduce SC load and assess their effect on CD4-Eomes differentiation.
  • Selective genetic deletion of the Eomes transcription factor in CD4 T cells in aged mice and liver cirrhosis models.

Main Results:

  • Reduction in SC load using senolytics halted CD4-Eomes differentiation.
  • Elimination of CD4-Eomes cells in aged mice led to increased SC accumulation, physical decline, and reduced lifespan.
  • In liver cirrhosis models, CD4-Eomes cell depletion exacerbated fibrosis and worsened disease severity.

Conclusions:

  • CD4-Eomes cells are crucial for modulating tissue senescence and mitigating age-related decline.
  • These findings reveal a fundamental immune mechanism influencing aging and longevity.
  • Targeting CD4-Eomes cells may offer therapeutic strategies for age-related diseases and extending healthspan.