Introduction: Autoimmune myasthenia gravis (MG) is a rare neuromuscular disease due to auto-antibodies that target acetylcholine receptors (AChRs) located at the neuromuscular junction (Gilhus, Tzartos et al. 2019). The AChR + MG patients are affected by muscle weakness and fatigue. The autoantibodies are produced in the ectopic germinal centers found in the thymus, the disease effector organ. Previous data showed that the cytokine IL 17 contributes actively to the pathogenic events occurring in thymus of AChR + MG patients (Villegas, Bayer et al. 2019) (Zhao, Luo et al. 2021). We then aimed to study whether IL-17 participates also to the pathogenic events occurring in the tissue targeted by the autoantibodies, the skeletal muscle. Materials and methods: The mRNA expression level and the tissue localization of IL-17A were assessed respectively by quantitative RT-PCR and immunohistochemistry in the classical experimental MG mouse model (EAMG) Results: mRNA analysis showed a significant increased expression of IL-17A in skeletal muscle of EAMG mice compared to controls mice. Surprisingly, the IHC analysis of skeletal muscle (tibialis anterior) revealed that IL-17 staining is located intra muscle fibers. In addition, the number of IL-17 positive fibers in the TA of EAMG mice, compared to control mice, is significantly increased. More, the analysis of IL-17A mRNA level in skeletal muscles of AChR + MG patients showed a similar increased expression compared to healthy control muscle biopsies. Conclusion: For the first time, we observed that skeletal muscles of EAMG mice and MG patients display an increased expression of the pro-inflammatory cytokine IL-17A. The role of IL-17 in the skeletal muscle is not so far clearly identified. Therefore, further investigations is required to understand the role and mechanism of action of IL-17 in the MG muscle.