Myasthenia gravis is an
autoimmune disease that affects skeletal muscle strength by impeding communication within the neuromuscular junction (NMJ). Research has shown that
sphingosine-1-phosphate (S1P)/
S1P receptor signaling may be involved in the process of
neuromuscular diseases.
Fingolimod is structurally similar to S1P, whose immunosuppressive effect has been recognized in many
immune diseases. However, the mechanism underlying
fingolimod's action on
experimental autoimmune myasthenia gravis is still far from clear. The aim of this study was to investigate the efficacy and possible mechanism of
fingolimod on
experimental autoimmune myasthenia gravis. Our results showed that pretreatment with
fingolimod improved
experimental autoimmune myasthenia gravis symptoms in a dose-dependent manner, including decreased anti-
acetylcholine receptor-2α
autoantibody titer, reduced compound muscle action potential decrement, and increased
acetylcholine receptor content. Further investigation indicated that
fingolimod inhibited lymphocyte proliferation responses and also regulated the balance of Th1/Th2 cells and Treg/Th17 cells. Moreover,
fingolimod suppressed the secretion of pro-inflammatory or inflammatory
cytokines IL-17A,
IL-6, and INF-γ, but did not noticeably alter the secretion of immunosuppressive
cytokines TGF-β1 and
IL-4. In conclusion, our results suggest that
fingolimod has a preventive effect on
experimental autoimmune myasthenia gravis by interfering with lymphocyte function.