Myasthenia gravis (MG) is an autoimmune disease due to auto-antibodies that attack acetylcholine receptors (AChRs) located at the neuromuscular junction. The AChR + MG patients are affected by muscle weakness and fatigability. Our previous data demonstrated that the pro-inflammatory cytokine, IL-17, contributes to maintain the chronic inflammation found in the thymus (the disease effector organ) and in the blood of MG patients. We investigated whether IL-17 participated also to the pathogenic events occurring in the muscle. Our data shown a significant increased expression of IL-17A in AChR + MG skeletal muscles compared to healthy controls. A similar observation was obtained in tibialis anterior of mice challenged with the AChR + MG experimental model (EAMG) compared to controls. Surprisingly, the immunohistochemistry analysis of skeletal muscles hihglited that IL-17 staining is not due to T cell infiltrates but due to muscle fibers. In addition, we found a significant increased number of IL-17 positive fibers in myasthenic individuals compared to controls in human as well as in EAMG mice. Finally, IL-17 expression level correlates with the disease clinical score in mice. These observations may suggest an active implication of IL-17 in skeletal muscle in the pathophysiological events occurring in MG individuals. Deeper investigations are required to define the roles and mechanisms of action of IL-17 in MG skeletal muscle.