Atorvastatin ameliorates experimental autoimmune neuritis by decreased Th1/Th17 cytokines and up-regulated T regulatory cells

► Atorvastatin administration could ameliorate EAN by immune regulation. ► Atorvastatin decreased the numbers of IFN-γ + and IL-17 + cells in sciatic nerves. ► Atorvastatin decreased the CD80 expression in lymph nodes mononuclear cells. ► Atorvastatin up-regulated the number of Treg cells. ► Atorvastatin decreased the levels of IFN-γ in MNC culture supernatants. Statins have anti-inflammatory and immune-regulating properties. To investigate the effects of atorvastatin on experimental autoimmune neuritis (EAN), an animal model of Guillain–Barré syndrome (GBS), atorvastatin was administered to Lewis rats immunized with bovine peripheral myelin in complete Freund’s adjuvant. We found that atorvastatin ameliorated the clinical symptoms of EAN, decreased the numbers of inflammatory cells as well as IFN-γ + and IL-17 + cells in sciatic nerves, decreased the CD80 expression and increased the number of CD25 +Foxp3 + cells in mononuclear cells (MNC), and decreased the levels of IFN-γ in MNC culture supernatants. These data provide strong evidence that atorvastatin can act as an inhibitor in EAN by inhibiting the immune response of Th1 and Th17, decreasing the expression of co-stimulatory molecule, and up-regulating the number of T regulatory cells. These data demonstrated that statins could be used as a therapeutic strategy in human GBS in future.