Published in:
Open Access
01-12-2014 | Research
Neuromyelitis optica MOG-IgG causes reversible lesions in mouse brain
Authors:
Samira Saadoun, Patrick Waters, Gregory P Owens, Jeffrey L Bennett, Angela Vincent, Marios C Papadopoulos
Published in:
Acta Neuropathologica Communications
|
Issue 1/2014
Login to get access
Abstract
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.