期刊
ACTA NEUROPATHOLOGICA COMMUNICATIONS
卷 2, 期 -, 页码 -出版社
BIOMED CENTRAL LTD
DOI: 10.1186/2051-5960-2-35
关键词
Antibody; Demyelination; Myelin oligodendrocyte glycoprotein; Neuromyelitis optica
资金
- Guthy Jackson Charitable Foundation
- Oxford NIHR Biomedical Research Centre
- NHS Specialised Services for NMO
- Guthy-Jackson Charitable Foundation
- NIH [EY022936, NS072141]
- NATIONAL EYE INSTITUTE [R01EY022936] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS072141] Funding Source: NIH RePORTER
Introduction: Antibodies against myelin oligodendrocyte glycoprotein (MOG-IgG) are present in some neuromyelitis optica patients who lack antibodies against aquaporin-4 (AQP4-IgG). The effects of neuromyelitis optica MOG-IgG in the central nervous system have not been investigated in vivo. We microinjected MOG-IgG, obtained from patients with neuromyelitis optica, into mouse brains and compared the results with AQP4-IgG. Results: MOG-IgG caused myelin changes and altered the expression of axonal proteins that are essential for action potential firing, but did not produce inflammation, axonal loss, neuronal or astrocyte death. These changes were independent of complement and recovered within two weeks. By contrast, AQP4-IgG produced complement-mediated myelin loss, neuronal and astrocyte death with limited recovery at two weeks. Conclusions: These differences mirror the better outcomes for MOG-IgG compared with AQP4-IgG patients and raise the possibility that MOG-IgG contributes to pathology in some neuromyelitis optica patients.
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