Treatment of experimental autoimmune myasthenia gravis rats with FTY720 and its effect on Th1/Th2 cells.

Abstract

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 4groups: Control group, Model group of experimental autoimmune myasthenia gravis (EAMG), 0.5mg/kg FTY720-treatment EAMG group and 1.0mg/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.