Myasthenia gravis (MG) is an autoimmune neurological disease that is characterized by the expression of anti-
acetylcholine receptor (AChR)
antibodies. The immune response at AChRs of neuromuscular junction is disrupted in patients with MG, which manifests as skeletal muscle
fatigue and is aggravated following periods of activity and alleviated following rest. Although a novel immune suppressant
FTY720 drug, which exhibits strong immune suppression efficacy and minor adverse effects, is available, its role and mechanism in MG have not been elucidated. The aim of this study was to investigate the role of
FTY720 in MG. A total of 60 healthy female Lewis rats were randomly assigned into 4 groups: Control group, Model group of
experimental autoimmune myasthenia gravis (EAMG), 0.5 mg/kg FTY720-treatment EAMG group and 1.0 mg/kg FTY720‑treatment EAMG group.
Body weight and symptoms were examined; Lennon score was used to evaluate improvement of clinical symptoms. Reverse transcription‑quantitative polymerase chain reaction and ELISA were used to test the
mRNA and
protein expression levels, respectively, of the helper T (Th)1 and Th2 cell
cytokines, including
interleukin (IL)‑2,
interferon (IFN)‑γ, IL‑4 and IL‑6 in thymus tissue and serum.
FTY720 treatment improved rat MG symptoms, increased
body weight and decreased Lennon score.
FTY720 treatments also reduced tissue and serum levels of IL‑2, IFN‑γ and IL‑6, but not IL‑4 expression levels.
FTY720 suppressed the inflammatory response and improved EAMG symptoms by inhibiting the secretion of inflammatory factors.