Student Author(s)

Harleen Saini

Academic Program


UMMS Affiliation

RNA Therapeutics Institute

Publication Date


Document Type



Molecular and Cellular Neuroscience | Nervous System Diseases | Neurology | Neuroscience and Neurobiology


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.


Neuromyelitis optica, Aquaporin-4, NMO-IgG, Astrocytes, Experimental autoimmune encephalomyelitis

Rights and Permissions

© 2013 Saini et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

DOI of Published Version



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

Journal/Book/Conference Title

BMC neurology

Related Resources

Link to article in PubMed

PubMed ID