These findings indicate that targeting the α-subunit impairs nAChR-dependent calcium signaling and can induce complement activation. Disrupted signaling and reduced nAChR levels were effectively restored by C3 inhibition, which blocks multiple downstream pathways; thus, terminal complement activation leading to MAC formation is a suggested, but it may not be the only mechanism. Overall, the results highlight C3 as a promising upstream therapeutic target and support combining subunit-specific interventions with proximal complement blockade in MG.
Radically different