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Myelin Oligodendrocyte Glycoprotein-IgG Contributes to Oligodendrocytopathy in the Presence of Complement, Distinct from Astrocytopathy Induced by AQP4-IgG.
- Source :
- Neuroscience Bulletin; Oct2019, Vol. 35 Issue 5, p853-866, 14p
- Publication Year :
- 2019
-
Abstract
- Immunoglobulin G against myelin oligodendrocyte glycoprotein (MOG-IgG) is detectable in neuromyelitis optica spectrum disorder (NMOSD) without aquaporin-4 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. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 16737067
- Volume :
- 35
- Issue :
- 5
- Database :
- Complementary Index
- Journal :
- Neuroscience Bulletin
- Publication Type :
- Academic Journal
- Accession number :
- 138724188
- Full Text :
- https://doi.org/10.1007/s12264-019-00375-8