Send to

Choose Destination
Mol Med. 2012 May 9;18:598-605. doi: 10.2119/molmed.2011.00471.

Statins induce the accumulation of regulatory T cells in atherosclerotic plaque.

Author information

The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China.


CD4⁺CD25⁺ regulatory T cells (Tregs) mediate immune suppression and prevent autoimmune disorders. Recently, Tregs were found to present in atherosclerotic lesions and play an important role in the progression of atherosclerosis. Statins have immunomodulatory properties, and the effect of statins on atherosclerosis depends in part on their immunomodulatory mechanisms. We sought to determine whether statins exhibit an effect on Tregs in atherosclerotic plaques and in peripheral circulation of patients with acute coronary syndrome (ACS). In an in vivo experiment, we induced atherosclerotic plaques in apolipoprotein E-deficient (ApoE⁻/⁻) mice. The mice were randomly divided into two groups for 6-wk treatment: simvastatin (50 mg/kg/d) or vehicle (control). Simvastatin significantly increased the number of Tregs and the expression of Treg marker Foxp3 (Forkhead/winged helix transcription factor), transforming growth factor (TGF)-β and interleukin (IL)-10 in atherosclerotic plaques. Moreover, simvastatin played an important role in modulating the balance between antiinflammatory (Tregs and Th2 cells) and proinflammatory (Th17 and Th1 cells) subsets of T cells. In an in vitro experiment, peripheral blood mononuclear cells (PBMCs) were isolated from patients with ACS and incubated with simvastatin. After an incubation for 96 h, simvastatin significantly enhanced the frequency and functional suppressive properties of Tregs. Therefore, statin treatment may influence Tregs in atherosclerotic lesions. Furthermore, statins improved the quantity and suppressive function of Tregs in ACS patients.

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Feinstein Institute Icon for PubMed Central
Loading ...
Support Center