ArticleScience translational medicine2017
Glucose-regulated protein 78 autoantibody associates with blood-brain barrier disruption in neuromyelitis optica.
Article in Science translational medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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Who cites it
78 citing papers in PubMed, 131 citations in OpenAlex.
- Autoantibodies against Neurologic Antigens in Nonneurologic Autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2019Trial
- Neutrophil extracellular traps exacerbate blood-brain barrier disruption in neuromyelitis optica spectrum disorder.Journal of neuroinflammation · 2026Article
- TRIM21 autoantibodies are associated with blood-brain barrier dysfunction in a subgroup of neuromyelitis optica spectrum disorder.Acta neuropathologica communications · 2026Article
- Endothelial Dysfunction: Insights into Systemic Lupus Erythematosus-associated Cardiovascular Disease and Neuropsychiatric Manifestations.Journal of cardiovascular translational research · 2026Review
- Article
- Diffuse neuropsychiatric lupus: Clinical evidence, immune-mediated mechanisms, and therapeutic insights.Seminars in immunology · 2025Review
- Restoring brain barriers: an innovative approach for treating neurological disorders.Fluids and barriers of the CNS · 2025Review
- Toward curing neurological autoimmune disorders: Biomarkers, immunological mechanisms, and therapeutic targets.Neuron · 2025Review
- Article
- The Involvement of Glial Cells in Blood-Brain Barrier Damage in Neuroimmune Diseases.International journal of molecular sciences · 2024Review
- Human cerebrospinal fluid monoclonal CASPR2 autoantibodies induce changes in electrophysiology, functional MRI, and behavior in rodent models.Brain, behavior, and immunity · 2024Article
- Blood-Brain Barrier Disruption in Neuroimmunological Disease.International journal of molecular sciences · 2024Review
- NMOSD and MOGAD: an evolving disease spectrum.Nature reviews. Neurology · 2024Review
- Modelling MOG antibody-associated disorder and neuromyelitis optica spectrum disorder in animal models: Spinal cord manifestations.Multiple sclerosis and related disorders · 2023Article
- Blood-Brain Barrier Breakdown in Neuroinflammation: Current In Vitro Models.International journal of molecular sciences · 2023Review
- Update on the diagnosis and treatment of neuromyelits optica spectrum disorders (NMOSD) - revised recommendations of the Neuromyelitis Optica Study Group (NEMOS). Part I: Diagnosis and differential diagnosis.Journal of neurology · 2023Review
- Paraneoplastic Neuromyelitis Optica Spectrum Disorder Related to Glucose-regulated Protein 78 (GRP78) Autoantibodies in a Patient with Lynch Syndrome-associated Colorectal Cancer.Internal medicine (Tokyo, Japan) · 2023Article
- Cell surface GRP78: a potential mechanism of therapeutic resistant tumors.Cancer cell international · 2023Review
- A narrative review of identifying the culprit antibody in neuroimmune diseases: concept and clinical significance.Annals of translational medicine · 2023Review
- Complement biomarkers reflect the pathological status of neuromyelitis optica spectrum disorders.Frontiers in immunology · 2023Article
18 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Neuromyelitis optica (NMO) is an inflammatory disorder mediated by antibodies to aquaporin-4 (AQP4) with prominent blood-brain barrier (BBB) breakdown in the acute phase of the disease. Anti-AQP4 antibodies are produced mainly in the periphery, yet they target the astrocyte perivascular end feet behind the BBB. We reasoned that an endothelial cell-targeted autoantibody might promote BBB transit of AQP4 antibodies and facilitate NMO attacks. Using monoclonal recombinant antibodies (rAbs) from patients with NMO, we identified two that strongly bound to the brain microvascular endothelial cells (BMECs). Exposure of BMECs to these rAbs resulted in nuclear translocation of nuclear factor κB p65, decreased claudin-5 protein expression, and enhanced transit of macromolecules. Unbiased membrane proteomics identified glucose-regulated protein 78 (GRP78) as the rAb target. Using immobilized GRP78 to deplete GRP78 antibodies from pooled total immunoglobulin G (IgG) of 50 NMO patients (NMO-IgG) reduced the biological effect of NMO-IgG on BMECs. GRP78 was expressed on the surface of murine BMECs in vivo, and repeated administration of a GRP78-specific rAb caused extravasation of serum albumin, IgG, and fibrinogen into mouse brains. Our results identify GRP78 antibodies as a potential component of NMO pathogenesis and GRP78 as a candidate target for promoting central nervous system transit of therapeutic antibodies.
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