Human in vitro neuromuscular junction model to functionally dissect the pathogenic mechanism of anti-AChR autoantibody-positive myasthenia gravis

These findings offer a mechanistic rationale for the observed clinical response in patients with anti-AChR autoantibody-positive myasthenia gravis treated with C5 inhibitors. The in vitro neuromuscular junction model provides a robust platform for studying the mechanistic pathways of complement-mediated damage and evaluating therapeutic interventions for myasthenia gravis.