Myasthenia gravis (MG) is an autoimmune disorder of neuromuscular transmission; this disease is primarily caused by autoantibodies specific to the human nicotinic acetylcholine receptor (AChR) and is characterized by fatigability and weakness of the striated muscles. Thymectomy and/or immunosuppressant therapy, particularly corticosteroid (CS) therapy, are commonly employed to improve the symptoms of MG and to prevent the destruction of the neuromuscular junction by AChR antibodies, although oral administration of anticholinesterase inhibitors is a useful adjunctive symptomatic therapy. However, a subset of MG patients do not show remission even after thymectomy and CS administration or cannot be administered sufficient doses of CSs because of the adverse effects of these drugs. Currently, MG is treated with several immunomodulating or immunosuppressive agents, including calcineurin inhibitors (CNIs) such as tacrolimus and cyclosporine. CNIs inhibit the calcium-calcineurin pathway thereby interfering with T-lymphocyte activation and transcription of inflammatory cytokine genes, including interleukin-2. CNIs have been successfully used for the treatment of transplantation patients and in several autoimmune disorders. Additionally, in vitro studies have indicated that tacrolimus may enhance the effects of CSs. Therefore, CNIs are expected to be effective in the treatment of autoimmune disorders, especially in the case of steroid-dependent patients. Herein, the current knowledge of the efficacy of CNIs in treating MG has been summarized.

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