Experimental Autoimmune Myasthenia Gravis (EAMG) remains a cornerstone platform for mechanistic studies of pathogenic antibodies in myasthenia gravis (MG). In particular, monoclonal antibody passive-transfer EAMG (mAb-PTMG) has been instrumental in establishing causal links between defined antibody specificities and downstream neuromuscular junction (NMJ) dysfunction, as well as in dissecting key mechanisms underlying AChR antibody–mediated disease. More recently, PTMG studies using patient-derived MuSK monoclonal antibodies have expanded the mechanistic landscape of MG and provided an in vivo framework for evaluating the efficacy and mechanisms of action of agonistic anti-MuSK therapeutic antibodies. In this review, we summarize practical considerations for monoclonal antibody sourcing and preparation, standardized experimental workflows, major readouts and their interpretation, and representative applications across MG subtypes. We also highlight emerging opportunities for model refinement and translational application, with the aim of supporting mechanism-guided interpretation and the development of targeted antibody therapies.
Zheng et al. (Fri,) studied this question.