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The effect of HMG-CoA reductase inhibitors on naturally occurring CD4+CD25+ T cells

Karin Mausner-Fainberg1, Galia Luboshits, Adi Mor

  • 1The Department of Cardiology, Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.

Atherosclerosis
|September 11, 2007
PubMed

Insights

Statins, widely used for lowering LDL cholesterol, may improve cardiovascular outcomes by boosting regulatory T cells (Tregs). Atorvastatin specifically increased functional Tregs in human blood, suggesting a novel immune mechanism for statin benefits.

Area of Science:

  • Immunology
  • Pharmacology
  • Cardiovascular Medicine

Background:

  • Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) are widely prescribed for their lipid-lowering effects and cardiovascular benefits.
  • Immune-mediated mechanisms are increasingly recognized as crucial to the therapeutic actions of statins, particularly in atherosclerosis.
  • CD4(+)CD25(+) regulatory T cells (Tregs) are vital for immune homeostasis, suppressing excessive immune responses and preventing inflammatory diseases.

Purpose of the Study:

  • To investigate the hypothesis that statins modulate the number and functional capacity of circulating regulatory T cells (Tregs).
  • To explore potential immune-based mechanisms underlying the clinical benefits of statin therapy.

Main Methods:

  • Human peripheral blood mononuclear cells (PBMCs) and murine cells were treated in vitro and in vivo with various statins (atorvastatin, mevastatin, pravastatin, simvastatin).
  • Flow cytometry was used to quantify Tregs (CD4(+)CD25(+)Foxp3(+)) and assess Foxp3 expression levels.
  • Co-culture experiments were performed to determine the origin of statin-induced Tregs.

Main Results:

  • In vitro treatment of human PBMCs with atorvastatin significantly increased the number of CD4(+)CD25(high) and CD4(+)CD25(+)Foxp3(+) Tregs.
  • Atorvastatin-induced Tregs exhibited enhanced regulatory function, with Foxp3 expression levels correlating positively with regulatory potential.
  • Simvastatin and pravastatin increased Treg numbers in hyperlipidemic human subjects, while statin treatment showed no effect on Tregs in C57BL/6 mice.

Conclusions:

  • Statins, particularly atorvastatin, can significantly expand the peripheral pool of functional Tregs in humans.
  • This statin-induced modulation of Tregs may represent a key mechanism contributing to their plaque-stabilizing and anti-inflammatory effects.
  • The observed effects on Tregs appear to be species-specific, with no significant impact noted in mice.

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