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.
Authors
- Baehyun Shin (ORCID: https://orcid.org/0000-0001-9892-5279)
- Jason E. Ekert (ORCID: https://orcid.org/0000-0003-4164-1640)
- Margaret H. Magdesian
- Eunja Kwon
- Douangsone D. Vadysirisack
- Camil E. Sayegh
- Miao Wang (ORCID: https://orcid.org/0000-0002-2661-3011)
- John H. Yim
Institutions
- Boston Children's Hospital (US)
- Advanced Micro Devices (Canada) (CA)
- Urban College of Boston (US)
- Bridge University (SS)
- Seva Mandir (IN)
- Novo Nordisk (United States) (US)
- Biota Pharmaceuticals (United States) (US)
- Roivant Sciences (United States) (US)
Publication Details
- Journal
- BMC Pharmacology and Toxicology
- Published
- 2025-12-12
- DOI
- https://doi.org/10.1186/s40360-025-01056-1
- Primary Topic
- Myasthenia Gravis and Thymoma
- Type
- article
- Field-Weighted Citation Impact
- 0.00