Safety profile and efficacy of secukinumab in the treatment of autoimmune myasthenia gravis: a single-center retrospective study.

Background: Myasthenia gravis (MG) is a chronic autoimmune disease caused by autoantibodies attacking the neuromuscular junction. Traditional treatments are often accompanied by side effects and lack specificity. Recent studies have found that Th17 cells and the inflammatory factor IL-17, which they secrete, play a key role in the pathogenesis of MG and have become potential therapeutic targets. Secukinumab, an IL-17 inhibitor, has shown efficacy in other autoimmune diseases, but its role in MG remains unexplored. Objective: This study aimed to evaluate the clinical efficacy and immunomodulatory effects of secukinumab in acetylcholine receptor antibody-positive generalized MG (AChR+ gMG). Methods: In this single-center retrospective study, 29 AChR+ gMG patients received subcutaneous secukinumab (150 mg weekly for 4 weeks, then monthly for 24 weeks). Clinical outcomes (QMG, MG-QOL15, MG-ADL scores), AChR antibody titers, Th17 cell frequency, and IL-17 levels were assessed at baseline and during treatment. Correlations between biomarkers and clinical improvements were analyzed. Results: By week 24, secukinumab treatment led to significant reductions in disease severity scores (QMG: 60.7%; MG-QOL15: 58.3%; MG-ADL: 64.1%) and AChR antibody levels (69.23%). Th17 cell frequency and IL-17 levels decreased by 68 and 84.47%, respectively. Strong baseline correlations were observed between IL-17, Th17, and clinical scores (r = 0.642-0.970, p < 0.001), with progressive uncoupling of these relationships during treatment. No severe adverse events were reported. Conclusion: Secukinumab demonstrated rapid and sustained clinical benefits in AChR+ gMG, linked to suppression of the Th17/IL-17 pathway. These findings highlight IL-17 inhibition as a promising targeted strategy for MG. Limitations include small sample size and retrospective design, warranting validation in larger randomized trials.