ArticlePloS one2011
Intravenous neuromyelitis optica autoantibody in mice targets aquaporin-4 in peripheral organs and area postrema.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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The trial behind it
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Who cites it
53 citing papers in PubMed, 89 citations in OpenAlex.
- Dissecting NMOSD pathogenesis through animal models: a mechanism-oriented systems perspective.Frontiers in immunology · 2026Review
- Antibodies in neurological diseases: Established, emerging, explorative.Immunological reviews · 2024Review
- Scientific issues with rodent models of neuromyelitis optic spectrum disorders.Frontiers in immunology · 2024Review
- Modelling MOG antibody-associated disorder and neuromyelitis optica spectrum disorder in animal models: Spinal cord manifestations.Multiple sclerosis and related disorders · 2023Article
- Neuromyelitis Optica Spectrum Disorder: From Basic Research to Clinical Perspectives.International journal of molecular sciences · 2022Review
- Autoimmune Neurogenic Dysphagia.Dysphagia · 2022Review
- Neuromyelitis optica spectrum disorders: from pathophysiology to therapeutic strategies.Journal of neuroinflammation · 2021Review
- Blood-brain barrier resealing in neuromyelitis optica occurs independently of astrocyte regeneration.The Journal of clinical investigation · 2021Article
- The Emerging Role of Microglia in Neuromyelitis Optica.Frontiers in immunology · 2021Review
- Induction of aquaporin 4-reactive antibodies in Lewis rats immunized with aquaporin 4 mimotopes.Acta neuropathologica communications · 2020Article
- Experimental animal models of aquaporin-4-IgG-seropositive neuromyelitis optica spectrum disorders: progress and shortcomings.Brain pathology (Zurich, Switzerland) · 2020Review
- Purified IgG from aquaporin-4 neuromyelitis optica spectrum disorder patients alters blood-brain barrier permeability.PloS one · 2020Article
- Unbalanced Expression of ICOS and PD-1 in Patients with Neuromyelitis Optica Spectrum Disorder.Scientific reports · 2019Article
- Membrane assembly of aquaporin-4 autoantibodies regulates classical complement activation in neuromyelitis optica.The Journal of clinical investigation · 2019Article
- CD55 upregulation in astrocytes by statins as potential therapy for AQP4-IgG seropositive neuromyelitis optica.Journal of neuroinflammation · 2019Article
- Circulating AQP4-specific auto-antibodies alone can induce neuromyelitis optica spectrum disorder in the rat.Acta neuropathologica · 2019Article
- Noninvasive, Targeted Creation of Neuromyelitis Optica Pathology in AQP4-IgG Seropositive Rats by Pulsed Focused Ultrasound.Journal of neuropathology and experimental neurology · 2019Article
- Transient Pulmonary Interstitial Lesions in Aquaporin-4-positive Neuromyelitis Optica Spectrum Disorder.Internal medicine (Tokyo, Japan) · 2018Article
- Paraneoplastic NMOSD associated with EG junction adenocarcinoma expressing unprotected AQP4.Neurology(R) neuroimmunology & neuroinflammation · 2018Article
- Mechanisms for lesion localization in neuromyelitis optica spectrum disorders.Current opinion in neurology · 2018Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The pathogenesis of neuromyelitis optica (NMO) involves binding of IgG autoantibodies (NMO-IgG) to aquaporin-4 (AQP4) on astrocytes in the central nervous system (CNS). We studied the in vivo processing in mice of a recombinant monoclonal human NMO-IgG that binds strongly to mouse AQP4. Following intravenous administration, serum [NMO-IgG] decreased with t(½) ∼18 hours in wildtype mice and ∼41 hours in AQP4 knockout mice. NMO-IgG was localized to AQP4-expressing cell membranes in kidney (collecting duct), skeletal muscle, trachea (epithelial cells) and stomach (parietal cells). NMO-IgG was seen on astrocytes in the area postrema in brain, but not elsewhere in brain, spinal cord, optic nerve or retina. Intravenously administered NMO-IgG was also seen in brain following mechanical disruption of the blood-brain barrier. Selective cellular localization was not found for control (non-NMO) IgG, or for NMO-IgG in AQP4 knockout mice. NMO-IgG injected directly into brain parenchyma diffused over an area of ∼5 mm² over 24 hours and targeted astrocyte foot-processes. Our data establish NMO-IgG pharmacokinetics and tissue distribution in mice. The rapid access of serum NMO-IgG to AQP4 in peripheral organs but not the CNS indicates that restricted antibody access cannot account for the absence of NMO pathology in peripheral organs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.