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Passively Transferred Human NMO-IgG Exacerbates Demyelination in Mouse Experimental Autoimmune Encephalomyelitis

Overview
Journal BMC Neurol
Publisher Biomed Central
Specialty Neurology
Date 2013 Aug 10
PMID 23927715
Citations 12
Authors
Affiliations
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Abstract

Background: Neuromyelitis optica (NMO) is a devastating inflammatory disorder of the optic nerves and spinal cord characterized by frequently recurring exacerbations of humoral inflammation. NMO is associated with the highly specific NMO-IgG biomarker, an antibody that binds the aquaporin-4 water channel. Aquaporin-4 is present on glial endfeet in the central nervous system (CNS). In humans, the NMO-IgG portends more frequent exacerbations and a worse long-term clinical outcome.

Methods: We tested the longer-term outcome of mice with EAE injected with NMO-IgG and followed them for 60 days. Clinical exams and pathology of the spinal cord and optic nerves were compared to mice that received control human IgG.

Results: Passively transferred human NMO-IgG leads to more severe neurology disability over two months after onset of disease. Clinical worsening is associated with an increased concentration of large demyelinating lesions primarily to subpial AQP4-rich regions of the spinal cord.

Conclusions: NMO-IgG is pathogenic in the context of EAE in mice.

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Low Frequency Ultrasound With Injection of NMO-IgG and Complement Produces Lesions Different From Experimental Autoimmune Encephalomyelitis Mice.

Xiang W, Xie C, Luo J, Zhang W, Zhao X, Yang H Front Immunol. 2021; 12:727750.

PMID: 34721390 PMC: 8551829. DOI: 10.3389/fimmu.2021.727750.


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