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Long-Term Alterations of Glucocorticoid Receptor Expression and CD4+ T Cells in Adolescent Rhesus Macaques Following

Mar M Sanchez1,2, Leonidas Panagiotakopoulos3, Timothy Hayes4

  • 1Department of Psychiatry & Behavioral Sciences, School of Medicine, Emory University, Atlanta, GA 30345, USA.

Biomolecules
|December 30, 2025
PubMed

Insights

Child maltreatment (MALT) causes lasting immune changes in adolescents. Early-life adversity impacts T cells and glucocorticoid receptor gene expression, affecting long-term health.

Area of Science:

  • Neuroscience
  • Immunology
  • Developmental Psychology

Background:

  • Child maltreatment (MALT) is a severe form of early-life adversity (ELA) with significant mental and physical health risks.
  • Disentangling the effects of postnatal caregiving from heritable factors in MALT research is challenging.

Purpose of the Study:

  • To investigate the long-term effects of MALT on immune function and inflammation in adolescence.
  • To control for biological/heritable factors using a cross-fostering design in a macaque model.

Main Methods:

  • Utilized a cross-fostering design in macaques to model MALT and control for genetic influences.
  • Assessed immunophenotype of peripheral blood mononuclear cells (PBMCs) and glucocorticoid receptor (GR) expression and function in adolescents exposed to MALT.
  • Analyzed changes in CD4+ T cell subsets (naïve and central memory).

Main Results:

  • MALT was associated with elevated expression of *NR3C1* (glucocorticoid receptor gene) in PBMCs.
  • Glucocorticoid receptor function, tested via dexamethasone (DEX) response, was not altered by MALT.
  • MALT exposure reduced naïve CD4+ T cells and increased central memory (Tcm) CD4+ T cells.

Conclusions:

  • Adolescents exposed to MALT exhibit persistent effects on CD4+ T cells and increased *NR3C1* expression.
  • Despite increased gene expression, glucocorticoid receptor function was not demonstrably enhanced by MALT.
  • Early-life adversity has enduring implications for cellular glucocorticoid receptor biology and T cell populations.

Keywords:
CD4+FKBP5TNFαchronic stressearly-life adversityglucocorticoid receptorhair cortisolnonhuman primate

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