【摘 要】
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Immunoglobulin G against myelin oligodendrocyte glycoprotein (MOG-IgG) is detectable in neuromyelitis optica spectrum disorder (NMOSD) without aquaporin4 IgG (AQP4-IgG),but its pathogenicity remains unclear.In this study,we explored the pathogenic mechani
【机 构】
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Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510000,
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Immunoglobulin G against myelin oligodendrocyte glycoprotein (MOG-IgG) is detectable in neuromyelitis optica spectrum disorder (NMOSD) without aquaporin4 IgG (AQP4-IgG),but its pathogenicity remains unclear.In this study,we explored the pathogenic mechanisms of MOG-IgG in vitro and in vivo and compared them with those of AQP4-IgG.MOG-IgG-positive serum induced complement activation and cell death in human embryonic kidney (HEK)-293T cells transfected with human MOG.In C57BL/6 mice and Sprague-Dawley rats,MOG-IgG only caused lesions in the presence of complement.Interestingly,AQP4-IgG induced astroglial damage,while MOG-IgG mainly caused myelin loss.MOG-IgG also induced astrocyte damage in mouse brains in the presence of complement.Importantly,we also observed ultrastructural changes induced by MOG-IgG and AQP4-IgG.These findings suggest that MOG-IgG directly mediates cell death by activating complement in vitro and producing NMOSD-like lesions in vivo.AQP4-IgG directly targets astrocytes,while MOG-IgG mainly damages oligodendrocytes.
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