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The increase of IFN-gamma production through aging correlates with the expanded CD8(+high)CD28(-)CD57(+)

E Bandrés1, J Merino, B Vázquez

  • 1School of Medicine, Clínica Universitaria, Pamplona, Spain.

Clinical Immunology (Orlando, Fla.)
|August 31, 2000
PubMed

Insights

Aging increases interferon-gamma (IFN-γ) production in CD8+ T cells, potentially linked to the CD8+CD28-CD57+ T-cell subset. This finding offers insights into immune system changes with age.

Area of Science:

  • Immunology
  • Cell Biology
  • Gerontology

Background:

  • Flow cytometry enables single-cell intracellular cytokine detection and phenotypic identification.
  • Imbalances in T-cell-derived intracellular cytokines are observed in pathological conditions.
  • Previous studies suggest aging may increase IFN-γ and IL-4 in healthy individuals.

Purpose of the Study:

  • To investigate IFN-γ and IL-4 production in CD4+ and CD8+ T cells across a wide age range (17-62 years).
  • To differentiate the effects of aging from chronic antigenic exposure on T-cell cytokine production.
  • To characterize the relationship between cytokine production and specific T-cell subpopulations.

Main Methods:

  • Flow cytometry was used to quantify intracellular IFN-γ and IL-4 in CD4+ and CD8+ T cells.
  • Multivariate analysis was employed to assess the impact of age and chronic antigenic exposure.
  • Phenotypic characterization of T cells, including CD28 and CD57 expression, was performed.

Main Results:

  • IFN-γ production in CD8+ T cells shows a direct correlation with increasing age.
  • Cytokine production is associated with the CD8+CD28-CD57+ T-cell population, which is elevated in aged individuals.
  • No significant correlation was found for IL-4 production with age or the studied T-cell subset.

Conclusions:

  • Aging is a significant factor influencing IFN-γ production in CD8+ T cells.
  • The CD8+CD28-CD57+ T-cell subset may play a regulatory role in the aging immune response, potentially as a Tc1 response.
  • Further research is needed to elucidate the regulatory mechanisms of this T-cell subpopulation in aging.

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