Immune signatures associated with human adrenocortical hypertension
Authors' conclusion
PA patients harbor autoreactive AT1R-specific CD8+ T cells that respond to aldosterone and cortisol through MR and GPER.
Study context
- Population
- Patients with confirmed primary aldosteronism (PA) and healthy donors
- Comparison
- PA vs healthy donors
- Outcome
- Presence of autoreactive AT1R-specific T cells and modulation of their activity by aldosterone or cortisol
Methodological detailsCortisol effects and 11βHSD2 expression examined, Peripheral blood mononuclear cells stimulated with overlapping AT1R peptides to identify autoreactive T cells, Chronic and rapid aldosterone effects on CD4+ and CD8+ T cells and receptors involved evaluated using mineralocorticoid receptor (MR) and G-protein estrogen receptor (GPER) antagonists, Functional cytotoxicity of AT1R-specific CD8+ clones toward human endothelial cells assessed
- Cortisol effects and 11βHSD2 expression examined
- Peripheral blood mononuclear cells stimulated with overlapping AT1R peptides to identify autoreactive T cells
- Chronic and rapid aldosterone effects on CD4+ and CD8+ T cells and receptors involved evaluated using MR and GPER antagonists
- Functional cytotoxicity of AT1R-specific CD8+ clones toward human endothelial cells assessed
Main finding
As reported in the abstract
- PA vs healthy donors: marked expansion of AT1R-specific CD8+ T cells recognizing the AFHYESQ epitope of the second extracellular AT1R loop
- AT1R-specific expansion not detected in CD4+ cells
- Both T-cell subsets expressed MR and GPER but lacked 11βHSD2 expression
- Chronic aldosterone exposure enhanced CD8+ proliferation and IFN-γ production through MR
- Rapid aldosterone stimulation activated CD8+ cells via MR and GPER
- In CD8+ cells cortisol also increased IFN-γ production through MR
- AT1R-specific CD8+ T-cell clones induced apoptosis of human endothelial cells expressing AT1R
Original publication
Immune signatures associated with human adrenocortical hypertension. Eur J Endocrinol. Published 7 September 2026. doi:10.
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