Dual effects of statins therapy in systemic lupus erythematosus and SLE-related atherosclerosis: The potential role for regulatory T cells

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease associated with accelerated atherosclerosis independent of traditional risk factors. Statins, the 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase inhibitors, have been widely prescribed for hyperlipidemia, which could slow the atherosclerosis progression, and reduce cardiovascular disease events. Nonetheless, accumulated evidences suggested that statins exert immunomodulatory and anti-inflammatory functions independent of their lipid-lowering effects. By the virtue of pleiotropic immunomodulatory property, statins may be applied for the treatment of both autoimmunity and atherosclerosis in patients with SLE. Interestingly, it has been well documented that regulatory T cells (Tregs) are involved in the pathogenesis of SLE as well as atherosclerosis. Meanwhile, studies have shown that statins could induce augmented number of Tregs with increased functional inhibitory properties. Thus, we hypothesized that the effect of statins ameliorating lupus disease manifestations and lupus-mediated atherogenesis might be mediated, at least partly, via the activation of Tregs.To our knowledge, this is the first hypothesis focused on that Tregs might be involved in the immunomodulatory effect of statins on SLE and SLE-related atherosclerosis.