Passively transferred human NMO-IgG exacerbates demyelination in mouse experimental autoimmune encephalomyelitis.
- Resource Type
- Article
- Authors
- Saini, Harleen; Rifkin, Robert; Gorelik, Michael; Huang, Hwa; Ferguson, Zachary; Jones, Melina V.; Levy, Michael
- Source
- BMC Neurology. 2013, Vol. 13 Issue 1, p1-9. 9p. 4 Color Photographs, 1 Chart, 2 Graphs.
- Subject
- *NERVES
*INFLAMMATION
*BIOMARKERS
*NEUROLOGY
*CRANIAL nerves
- Language
- ISSN
- 1471-2377
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. [ABSTRACT FROM AUTHOR]