There are very few studies in which MuSK autoantibody–producing B cells have been isolated, but these B cells have been found in the circulation and have a memory B cell or short-lived plasmablasts phenotype. MuSK MG develops via autoantibodies with the IgG subclass IgG4 — which, unlike other subclasses, can undergo Fab-arm exchange — thereby directly disrupting AChR signaling by hindering NMJ protein-protein interactions.
It is theorized that the mechanism used by B cells for autoantibody production differs between AChR MG and MuSK MG. AChR MG is characterized by the complement-activating IgG subclasses IgG1, IgG2, and IgG3, produced by plasma cells residing in tissues such as the bone marrow and thymus, with effector functions that can cause tissue damage at the NMJ. It is also widely theorized that AChR-specific autoantibodies stem from long-lived plasma cells.
Learn more about the pathophysiology of MG.
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Cite this: Raghav Govindarajan. Fast Five Quiz: Pathophysiology of Myasthenia Gravis - Medscape - Oct 08, 2021.