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Aging is associated with increased regulatory T-cell function.

Sanjay K Garg1, Colin Delaney, Tomomi Toubai

  • 1Division of Geriatrics and Palliative Medicine, Ann Arbor, MI-48109, USA.

Aging Cell
|December 12, 2013
PubMed
Summary
This summary is machine-generated.

Aged mice show increased regulatory T-cell (Treg) numbers and function, with hypomethylated DNA enhancing FoxP3 expression. These Tregs exhibit heightened immune suppression, potentially contributing to age-related disease susceptibility.

Keywords:
agingepigeneticsmethylationredoxregulatory T cell

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Area of Science:

  • Immunology
  • Aging Research
  • Cellular Biology

Background:

  • Immune senescence increases disease susceptibility with age.
  • Regulatory T-cells (Tregs) play a crucial role in immune regulation.
  • FoxP3 is a key regulator of Treg function, influenced by epigenetic modifications.

Purpose of the Study:

  • To investigate age-related changes in FoxP3 expression and Treg function in C57BL/6 mice.
  • To explore the epigenetic mechanisms underlying Treg alterations in aging.
  • To determine how aged Tregs impact effector T-cell (Teff) proliferation and immune suppression.

Main Methods:

  • Comparison of FoxP3 expression and DNA methylation in CD4+ T cells from young and aged mice.
  • In vitro co-culture assays to assess Treg-mediated suppression of Teff proliferation.
  • Analysis of cytokine production (IL-10) and cell surface marker expression (CD86) on dendritic cells (DCs).

Main Results:

  • Aged mice exhibited hypomethylated CD4+ T-cell DNA, increased Treg numbers, and higher FoxP3 expression.
  • Tregs from aged mice demonstrated enhanced suppression of Teff proliferation in vitro.
  • Aged Tregs showed greater redox remodeling-mediated suppression and stronger inhibition of CD86 expression on DCs, alongside higher IL-10 production.

Conclusions:

  • Epigenetic changes, specifically hypomethylation, contribute to increased FoxP3 expression and Treg activity in aged mice.
  • Enhanced Treg-mediated immune suppression in aged individuals may be a significant factor in age-related immune dysfunction.
  • These findings reveal a potential mechanism for increased immune suppression with advancing age.