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L.L. Kusner, C. Richmonds, H. Kaminski; Pathological Analysis of Extraocular Muscle in Active Induction Myasthenia Gravis . Invest. Ophthalmol. Vis. Sci. 2005;46(13):5728.
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Purpose: In humans, myasthenia gravis (MG) demonstrates a predilection for clinical involvement of extraocular muscles (EOM), but no studies exist characterizing the pathology of EOM in myasthenia gravis or the animal model, autoimmune experimental MG (EAMG). In this investigation we compare complement, IgG deposition, and ultrastructural alterations at EOM and diaphragm neuromuscular junctions. Methods: EAMG was induced by administration of purified Torpedo acetylcholine receptor (AChR) to 8–12 week old C57black mice at day 0 and 30. On day 45 mice were sacrificed, EOM and diaphragm harvested for C3 and IgG deposition as well as ultrastructural analysis. Neuromuscular junctions were identified by Texas Red bungarotoxin and a minimum of 50 junctions were evaluated for IgG or C3 deposition. Serum was assayed for AChR antibody. Results: All mice demonstrated mild to moderate general weakness, but no behavioral deficits of ocular function. All had elevated serum AChR antibody. In the 5 of 6 animals evaluated the percentage of EOM junctions with IgG and C3 deposits was greater than that of diaphragm junctions. In one animal all junctions of EOM and diaphragm had IgG and C3 deposits. Ultrastructurally, EOM junctions demonstrated more significant injury. Conclusions: EOM of mice with EAMG demonstrate greater degrees of damage as well as complement and IgG deposition. As in human MG, the EOM appear to be more susceptible to EAMG, and previous studies suggest that lower expression of complement regulators may contribute to this differential susceptibility.
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