Dual effects of statins therapy in systemic lupus erythematosus and SLE-related atherosclerosis: The potential role for regulatory T cells
Tu H et al. – Authors 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.
- 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.