Passively transferred human NMO-IgG exacerbates demyelination in mouse experimental autoimmune encephalomyelitis
Saini, Harleen Rifkin, Robert Gorelik, Michael Huang, Hwa Ferguson, Zachary Jones, Melina V. Levy, Michael
Citations
Student Authors
Faculty Advisor
Academic Program
UMass Chan Affiliations
Document Type
Publication Date
Subject Area
Collections
Embargo Expiration Date
Link to Full Text
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.
Source
Saini H, Rifkin R, Gorelik M, Huang H, Ferguson Z, Jones MV, Levy M. Passively transferred human NMO-IgG exacerbates demyelination in mouse experimental autoimmune encephalomyelitis. BMC Neurol. 2013 Aug 8;13:104. doi: 10.1186/1471-2377-13-104. Link to article on publisher's site