ArticleActa neuropathologica communications2017
Complement regulator CD59 prevents peripheral organ injury in rats made seropositive for neuromyelitis optica immunoglobulin G.
Article in Acta neuropathologica communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- CRISPR and Myelin regeneration: a systematic review of applications in demyelinating CNS Disorders, with a focus on MS.Regenerative medicine · 2025Pooled it
- Ravulizumab in NMOSD with associated interstitial pneumonitis in a 59-year-old female patient: a case report.Frontiers in immunology · 2025Article
- Complement activation in immunological neurological disorders: mechanisms and therapeutic strategies.Frontiers in neurology · 2025Review
- Effect of Heme Oxygenase-1 Depletion on Complement Regulatory Proteins Expression in the Rat.Antioxidants (Basel, Switzerland) · 2022Article
- Immuno-pathogenesis of neuromyelitis optica and emerging therapies.Seminars in immunopathology · 2022Review
- Neuromyelitis Optica Spectrum Disorder: From Basic Research to Clinical Perspectives.International journal of molecular sciences · 2022Review
- Neuromyelitis Optica Spectrum Disorder Treatment-Current and Future Prospects.International journal of molecular sciences · 2021Review
- Advances in Genome Editing and Application to the Generation of Genetically Modified Rat Models.Frontiers in genetics · 2021Review
- Autoantibodies Against the Complement Regulator Factor H in the Serum of Patients With Neuromyelitis Optica Spectrum Disorder.Frontiers in immunology · 2021Article
- Can Immune Tolerance Be Re-established in Neuromyelitis Optica?Frontiers in neurology · 2021Review
- Complement in neurological disorders and emerging complement-targeted therapeutics.Nature reviews. Neurology · 2020Review
- Interleukin-6 in neuromyelitis optica spectrum disorder pathophysiology.Neurology(R) neuroimmunology & neuroinflammation · 2020Review
- Experimental animal models of aquaporin-4-IgG-seropositive neuromyelitis optica spectrum disorders: progress and shortcomings.Brain pathology (Zurich, Switzerland) · 2020Review
- B cells in autoimmune and neurodegenerative central nervous system diseases.Nature reviews. Neuroscience · 2019Review
- 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
- Noninvasive, Targeted Creation of Neuromyelitis Optica Pathology in AQP4-IgG Seropositive Rats by Pulsed Focused Ultrasound.Journal of neuropathology and experimental neurology · 2019Article
- Article
- The evolving mystery of why skeletal muscle is spared in seropositive neuromyelitis optica.Journal of cellular and molecular medicine · 2018Article
- Comprehensive review of neuromyelitis optica and clinical characteristics of neuromyelitis optica patients in Puerto Rico.Surgical neurology international · 2018Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Pathogenesis in aquaporin-4 immunoglobulin G (AQP4-IgG) seropositive neuromyelitis optica spectrum disorders (herein called NMO) involves complement-dependent cytotoxicity initiated by AQP4-IgG binding to astrocyte AQP4. We recently reported that rats lacking complement inhibitor protein CD59 were highly susceptible to development of NMO pathology in brain and spinal cord following direct AQP4-IgG administration (Yao and Verkman, Acta Neuropath Commun 2017, 5:15). Here, we report evidence that CD59 is responsible for protection of peripheral, AQP4-expressing tissues in seropositive NMO. Rats made seropositive by intraperitoneal injection of AQP4-IgG developed marked weakness by 24 h and died soon thereafter. Serum creatine phosphokinase at 24 h was >900-fold greater in seropositive CD59
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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.