December 1, 1981Annals of the New York Academy of Sciences
Monoclonal Autoantibodies to Acetylcholine Receptors: Evidence for a Dominant Idiorpe and Requirement of Complement for Pathogenicity*
Population
Rats and living myotubes in culture used as models for experimental autoimmune myasthenia gravis
Comparison
Four IgG monoclonal autoantibodies to… vs Complement-deficient states
Design
Preclinical
Follow-up
72 hours (for in vivo binding experiment)
Authors
Discussion
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Implication
Highlights complement as essential for McAb-induced neuromuscular impairment in EAMG; leaves open translation to human myasthenia gravis.
Structured PICO
P
Population
Rats (donor rats, and rats immunized with AChR of Torpedo, eel or syngeneic muscle) and living myotubes in culture used as models for experimental autoimmune myasthenia gravis (EAMG)
I
Intervention
Four IgG monoclonal autoantibodies (McAb's) to acetylcholine receptors (AChR) and anti-idiotype (anti-Id) antibodies
C
Comparator
Complement-deficient states (absence of C3 to C9, or isolated deficiency of C4)
O
Outcome
Induction of experimental autoimmune myasthenia gravis (EAMG) and impairment of neuromuscular transmission (measured by miniature endplate potentials [MEPPs] and EPPs)surrogate
Monoclonal autoantibodies to acetylcholine receptors require classical complement pathway activation to impair neuromuscular transmission in experimental autoimmune myasthenia gravis.
Cite This Study
Lennon et al. (1981) studied this question.