Seronegative myasthenia gravis (MuSK-antibody positive) differs from classic AChR-antibody MG in which pathological mechanism?
- A Complement-mediated destruction of the neuromuscular junction
- B T-cell mediated destruction of motor neurons in the anterior horn
- C Type III immune complex deposition in the NMJ basement membrane
- D Blocking of acetylcholine binding without complement activation; also involving disruption of AChR clustering at the NMJ ✓
Explanation
Anti-MuSK (muscle-specific kinase) antibodies are predominantly IgG4, which does not fix complement. They block MuSK, a receptor tyrosine kinase essential for agrin-mediated clustering of AChRs at the NMJ, thereby disrupting NMJ architecture without complement-mediated lysis. Classic AChR antibody MG involves complement activation and AChR downregulation/destruction. MuSK MG has distinct clinical features including more prominent bulbar and facial involvement.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.