ArticleAnnals of neurology2009
Neuromyelitis optica: pathogenicity of patient immunoglobulin in vivo.
Article in Annals of neurology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 249 papers.
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Who cites it
249 citing papers in PubMed, 557 citations in OpenAlex.
- Serum Glial Fibrillary Acidic Protein: A Neuromyelitis Optica Spectrum Disorder Biomarker.Annals of neurology · 2021Trial
- Complement C3 inhibitory peptide AMY-101 ameliorates brain injury in a mouse model of NMOSD.Annals of medicine · 2026Article
- Dynamic characterization of pathological and functional deterioration in a mouse model of optic neuritis related to neuromyelitis optica spectrum disorder.Neural regeneration research · 2026Article
- Narcolepsy is (not) an autoimmune disease.Nature reviews. Neurology · 2026Review
- Progress on experimental models of neuromyelitis optica spectrum disease.IBRO neuroscience reports · 2026Review
- Integrated Blood Inflammatory Ratios and Cerebrospinal Fluid Blood‒Brain Barrier Dysfunction Predict Relapse Risk in Neuromyelitis Optica Spectrum Disorder.Brain and behavior · 2026Article
- Endothelial cell-secreted SPARC suppresses astrocytic CD59 expression and promotes astrocytopathy in a mouse model of neuromyelitis optica spectrum disorders.Nature communications · 2026Article
- Causal Exposures of Immune Cells in Neuromyelitis Optica Spectrum Disorders: A Mendelian Randomization Study and Flow Cytometry Analysis.Brain and behavior · 2026Article
- Complement C4d Informs the Differential Diagnosis of Inflammatory Demyelinating CNS Diseases.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- Natalizumab exacerbates astrocytopathy in NMOSD via blockade of endothelial VCAM1-astrocytic integrin α4 interaction.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Dissecting NMOSD pathogenesis through animal models: a mechanism-oriented systems perspective.Frontiers in immunology · 2026Review
- Inflammatory transcriptomic signatures in a human cellular NMOSD model reveal upregulation of NF-κB and IL6 pathways.Scientific reports · 2025Article
- Ophthalmological manifestations in autoimmune diseases: Overcoming diagnostic and therapeutic challenges.World journal of experimental medicine · 2025Review
- Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: Pathophysiology, Clinical Patterns, and Therapeutic Challenges of Intractable and Severe Forms.International journal of molecular sciences · 2025Review
- Friend or foe: assessing the value of animal models for facilitating clinical breakthroughs in complement research.The Journal of clinical investigation · 2025Review
- Aquaporin-4 Peptide Injection in Mice Induces Retinal and Optic Nerve Alterations That Simulate Those of Neuromyelitis Optica Spectrum Disorder.Translational vision science & technology · 2025Article
- AQP4-specific T cells determine lesion localization in the CNS in a model of NMOSD.Acta neuropathologica communications · 2025Article
- Toward curing neurological autoimmune disorders: Biomarkers, immunological mechanisms, and therapeutic targets.Neuron · 2025Review
- "Lupus Myelitis" Revisited: A Retrospective Single-Center Study of Myelitis Associated With Rheumatologic Disease.Neurology(R) neuroimmunology & neuroinflammation · 2025Article
- Myelin Oligodendrocyte Glycoprotein Antibody-Associated Optic Neuritis Following SARS-CoV-2 Vaccination.Cureus · 2025Article
189 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveSevere inflammation and astrocyte loss with profound demyelination in spinal cord and optic nerves are typical pathological features of neuromyelitis optica (NMO). A diagnostic hallmark of this disease is the presence of serum autoantibodies against the water channel aquaporin-4 (AQP-4) on astrocytes.
methodsWe induced acute T-cell-mediated experimental autoimmune encephalomyelitis in Lewis rats and confronted the animals with an additional application of immunoglobulins from AQP-4 antibody-positive and -negative NMO patients, multiple sclerosis patients, and control subjects.
resultsThe immunoglobulins from AQP-4 antibody-positive NMO patients are pathogenic. When they reach serum titers in experimental animals comparable with those seen in NMO patients, they augment clinical disease and induce lesions in the central nervous system that are similar in structure and distribution to those seen in NMO patients, consisting of AQP-4 and astrocyte loss, granulocytic infiltrates, T cells and activated macrophages/microglia cells, and an extensive immunoglobulin and complement deposition on astrocyte processes of the perivascular and superficial glia limitans. AQP-4 antibody containing NMO immunoglobulin injected into naïve rats, young rats with leaky blood-brain barrier, or after transfer of a nonencephalitogenic T-cell line did not induce disease or neuropathological alterations in the central nervous system. Absorption of NMO immunoglobulins with AQP-4-transfected cells, but not with mock-transfected control cells, reduced the AQP-4 antibody titers and was associated with a reduction of astrocyte pathology after transfer.
interpretationHuman anti-AQP-4 antibodies are not only important in the diagnosis of NMO but also augment disease and induce NMO-like lesions in animals with T-cell-mediated brain inflammation.
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