The DOI matches its Crossref record; 28 of the 28 references it cites were found in a registry or an index.
Pathogenic potential of IgG binding to water channel extracellular domain in neuromyelitis optica
Abstract
BACKGROUND: Autoantibody specific for the aquaporin-4 astrocytic water channel is restricted to serum and CSF of patients with neuromyelitis optica (NMO) and related CNS inflammatory demyelinating disorders (relapsing optic neuritis and longitudinally extensive transverse myelitis). NMO-typical lesions are distinct from MS-typical lesions. Aquaporin-4 is lost selectively at vasculocentric sites of edema/inflammation coinciding with focal deposits of immunoglobulins (Ig) G, M, and terminal complement products, with and without myelin loss. Evidence for antigen-specific autoantibody pathogenicity is lacking. METHODS: We used confocal microscopy and flow cytometry to evaluate the selectivity and immunopathological consequences of Ig binding to surface epitopes of living target cells expressing aquaporin-4 fused at its cytoplasmic N-terminus with GFP. We tested serum, IgG-enriched and IgG-depleted serum fractions, and CSF from patients with NMO, neurologic control patients, and healthy subjects. We also analyzed aquaporin-4 immunoreactivity in myelinated adult mouse optic nerves and spinal cord, and plasma cell Ig isotypes in archived brain tissue from an NMO patient. RESULTS: Serum IgG from patients with NMO binds to the extracellular domain of aquaporin-4; it is predominantly IgG(1), and it initiates two potentially competing outcomes, aquaporin-4 endocytosis/degradation and complement activation. Serum and CSF lack aquaporin-4-specific IgM, and plasma cells in CNS lesions of NMO contain only IgG. Paranodal astrocytic endfeet highly express aquaporin-4. CONCLUSIONS: NMO patients' serum IgG has a selective pathologic effect on cell membranes expressing aquaporin-4. IgG targeting astrocytic processes around nodes of Ranvier could initiate demyelination.
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Cites
Astrocyte-endothelial interactions at the blood-brain barrier
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A serum autoantibody marker of neuromyelitis optica: distinction from multiple sclerosis
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Self-citationWalport, M. J. (2001) · New England Journal of Medicine · doi:10.1056/nejm200104053441406 · Cited by 2,927
IgG marker of optic-spinal multiple sclerosis binds to the aquaporin-4 water channel
Lennon, V. A., Kryzer, T. J., Pittock, S. J., Verkman, A. S., & Hinson, S. R. (2005) · The Journal of Experimental Medicine · doi:10.1084/jem.20050304 · Cited by 2,288
Self-citationRaff, M. C., Miller, R. H., & Noble, M. (1983) · Nature · doi:10.1038/303390a0 · Cited by 2,030
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A role for humoral mechanisms in the pathogenesis of Devic's neuromyelitis optica
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Self-citationGlutamate excitotoxicity in a model of multiple sclerosis
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The molecular basis of water transport in the brain
Amiry-Moghaddam, M., & Ottersen, O. P. (2003) · Nature Reviews Neuroscience · doi:10.1038/nrn1252 · Cited by 733
Roemer, S. F., Parisi, J. E., Lennon, V. A., Benarroch, E. E., Lassmann, H., Bruck, W., Mandler, R. N., Weinshenker, B. G., Pittock, S. J., Wingerchuk, D. M., et al. (2007) · Brain · doi:10.1093/brain/awl371 · Cited by 716
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Development, maintenance and disruption of the blood-brain barrier
Obermeier, B., Daneman, R., & Ransohoff, R. M. (2013) · Nature Medicine · doi:10.1038/nm.3407 · Cited by 2,452
Aquaporins: important but elusive drug targets
Verkman, A. S., Anderson, M. O., & Papadopoulos, M. C. (2014) · Nature Reviews Drug Discovery · doi:10.1038/nrd4226 · Cited by 586
Serologic diagnosis of NMO: A multicenter comparison of aquaporin-4-IgG assays
Waters, P. J., McKeon, A., Leite, M. I., Rajasekharan, S., Lennon, V. A., Villalobos, A., Palace, J., Mandrekar, J. N., Vincent, A., Bar-Or, A., et al. (2012) · Neurology · doi:10.1212/wnl.0b013e318248dec1 · Cited by 526
Self-citationJarius, S., Paul, F., Weinshenker, B. G., Levy, M., Kim, H. J., & Wildemann, B. (2020) · Nature Reviews Disease Primers · doi:10.1038/s41572-020-0214-9 · Cited by 478
Hinson, S. R., Roemer, S. F., Lucchinetti, C. F., Fryer, J. P., Kryzer, T. J., Chamberlain, J. L., Howe, C. L., Pittock, S. J., & Lennon, V. A. (2008) · The Journal of Experimental Medicine · doi:10.1084/jem.20081241 · Cited by 355
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Metadata
- Authors
- Hinson, S. R., Pittock, S. J., Lucchinetti, C. F., Roemer, S. F., Fryer, J. P., Kryzer, T. J., & Lennon, V. A.
- Venue
- Neurology
- Published
- 2007-12-11
- Volume
- 69
- Issue
- 24
- Pages
- 2221-2231
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- OpenAlex
- W2067927161
- Cited by
- 494
- References
- 28
- FWCI
- 19.27
- Type
- journal article
- Language
- en
- Open access
- closed
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- Hinson, S. R., Pittock, S. J., Lucchinetti, C. F., Roemer, S. F., Fryer, J. P., Kryzer, T. J., & Lennon, V. A. (2007). Pathogenic potential of IgG binding to water channel extracellular domain in neuromyelitis optica. Neurology. https://doi.org/10.1212/01.wnl.0000289761.64862.ce
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