ArticleJournal of neuroinflammation2016
Complement-independent retinal pathology produced by intravitreal injection of neuromyelitis optica immunoglobulin G.
Article in Journal of neuroinflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- AQP4-IgG and MOG-IgG Related Optic Neuritis-Prevalence, Optical Coherence Tomography Findings, and Visual Outcomes: A Systematic Review and Meta-Analysis.Frontiers in neurology · 2020Pooled it
- Dynamic characterization of pathological and functional deterioration in a mouse model of optic neuritis related to neuromyelitis optica spectrum disorder.Neural regeneration research · 2026Article
- Microglial PD-1/PD-L1 axis in CNS demyelinating diseases: a dual immunoregulatory perspective.Frontiers in cellular neuroscience · 2026Review
- Dissecting NMOSD pathogenesis through animal models: a mechanism-oriented systems perspective.Frontiers in immunology · 2026Review
- PPAR-γ activation by pioglitazone inhibits microglia-mediated neuroinflammation and alleviates disease in neuromyelitis optica spectrum disorders.Acta neuropathologica communications · 2025Article
- Umbilical Cord Mesenchymal Stromal Cell-Derived Extracellular Vesicles Transfer CD59 to Astrocytes to Alleviate Complement-Dependent Cytotoxicity.Molecular neurobiology · 2025Article
- Smoking status and vascular risk factors as predictors of disability in AQP4-NMOSD and MOGAD.Multiple sclerosis (Houndmills, Basingstoke, England) · 2025Article
- Intravitreal delivery of NMO-IgG causes primary retinal damage in the absence of optic nerve injury.Journal of neuroinflammation · 2025Article
- Stage-dependent immunity orchestrates AQP4 antibody-guided NMOSD pathology: a role for netting neutrophils with resident memory T cells in situ.Acta neuropathologica · 2024Article
- hUC-MSCs-derived MFGE8 ameliorates locomotor dysfunction via inhibition of ITGB3/ NF-κB signaling in an NMO mouse model.NPJ Regenerative medicine · 2024Article
- Scientific issues with rodent models of neuromyelitis optic spectrum disorders.Frontiers in immunology · 2024Review
- NMOSD IgG Impact Retinal Cells in Murine Retinal Explants.Current issues in molecular biology · 2023Article
- Inhibition of complement C3 signaling ameliorates locomotor and visual dysfunction in autoimmune inflammatory diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Modeling MOG Antibody-Associated Disorder and Neuromyelitis Optica Spectrum Disorder in Animal Models: Visual System Manifestations.Neurology(R) neuroimmunology & neuroinflammation · 2023Article
- Active Transport and Ocular Distribution of Intravitreally Injected Liposomes.Translational vision science & technology · 2023Article
- T follicular helper cells contribute to pathophysiology in a model of neuromyelitis optica spectrum disorders.JCI insight · 2023Article
- Structure-function correlates of vision loss in neuromyelitis optica spectrum disorders.Scientific reports · 2022Article
- Neuromyelitis Optica Spectrum Disorder: From Basic Research to Clinical Perspectives.International journal of molecular sciences · 2022Review
- Spectrum of sublytic astrocytopathy in neuromyelitis optica.Brain : a journal of neurology · 2022Article
- Retinal Optical Coherence Tomography in Neuromyelitis Optica.Neurology(R) neuroimmunology & neuroinflammation · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundNeuromyelitis optica (NMO), an autoimmune inflammatory disease of the central nervous system, is often associated with retinal abnormalities including thinning of the retinal nerve fiber layer and microcystic changes. Here, we demonstrate that passive transfer of an anti-aquaporin-4 autoantibody (AQP4-IgG) produces primary retinal pathology.
methodsAQP4-IgG was delivered to adult rat retinas by intravitreal injection. Rat retinas and retinal explant cultures were assessed by immunofluorescence.
resultsImmunofluorescence showed AQP4-IgG deposition on retinal Müller cells, with greatly reduced AQP4 expression and increased glial fibrillary acidic protein by 5 days. There was mild retinal inflammation with microglial activation but little leukocyte infiltration and loss of retinal ganglion cells by 30 days with thinning of the ganglion cell complex. Interestingly, the loss of AQP4 was complement independent as seen in cobra venom factor-treated rats and in normal rats administered a mutated AQP4-IgG lacking complement effector function. Exposure of ex vivo retinal cultures to AQP4-IgG produced a marked reduction in AQP4 expression by 24 h, which was largely prevented by inhibitors of endocytosis or lysosomal acidification.
conclusionsPassive transfer of AQP4-IgG results in primary, complement-independent retinal pathology, which might contribute to retinal abnormalities seen in NMO patients.
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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.