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PPARgamma Deficiency Counteracts Thymic Senescence.

David Ernszt1,2, Krisztina Banfai1,2, Zoltan Kellermayer3

  • 1Faculty of Pharmacy, Department of Pharmaceutical Biotechnology, University of Pecs, Pecs, Hungary.

Frontiers in Immunology
|November 23, 2017
PubMed
Summary

Decreasing PPARgamma activity delays thymic senescence, enhancing T-cell production and immune function in aging. This approach may combat age-related immune decline but carries metabolic risks.

Keywords:
PPARgammaimmunityrejuvenationsenescencethymus

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Area of Science:

  • Immunology
  • Aging Research
  • Metabolic Regulation

Background:

  • Thymic senescence, marked by adipose involution, increases susceptibility to infections, cancer, and autoimmunity in older individuals.
  • Thymic adipose involution is regulated by Peroxisome proliferator-activated receptor gamma (PPARgamma), similar to other adipose tissues.
  • Systemic activation of PPARgamma accelerates thymic adipose involution, suggesting its inhibition could counteract senescence.

Purpose of the Study:

  • To investigate whether decreased PPARgamma activity can prevent thymic adipose involution and senescence.
  • To evaluate the impact of reduced PPARgamma activity on immune function and metabolic parameters in aging.
  • To explore the potential of targeting PPARgamma for therapeutic interventions against age-related immune decline.

Main Methods:

  • Analysis of PPARgamma expression in human and murine thymic sections.
  • Assessment of thymic senescence in PPARgamma haplo-insufficient and null mice using histology, qPCR for T-cell recombination, and flow cytometry for naive T-cell ratios.
  • Evaluation of functional immune parameters, including oral tolerance and vaccine response, in senior PPARgamma haplo-insufficient mice.
  • Comparison of thymic senescence markers in human patients with FPLD3 (PPARgamma haplo-insufficiency) versus matched controls.

Main Results:

  • PPARgamma haplo-insufficient and null mice exhibited delayed thymic senescence, with a dose-response relationship to PPARgamma deficiency.
  • Senior PPARgamma haplo-insufficient mice demonstrated sustained T-cell production, leading to improved oral tolerance and enhanced vaccination efficiency.
  • Human patients with FPLD3 showed increased hTrec values, suggesting delayed thymic senescence, aligning with mouse findings.
  • PPARgamma deficiency was associated with metabolic adverse effects, particularly in null mice and FPLD3 patients.

Conclusions:

  • Systemic reduction of PPARgamma activity effectively prevents thymic senescence and preserves immune function in aging.
  • While beneficial for immunity, decreased PPARgamma activity presents metabolic drawbacks.
  • Targeting PPARgamma specifically within the thymus could offer a therapeutic strategy to mitigate age-related immune decline without systemic metabolic side effects.