ArticleActa neuropathologica communications2020
Induction of aquaporin 4-reactive antibodies in Lewis rats immunized with aquaporin 4 mimotopes.
Article in Acta neuropathologica communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Dissecting NMOSD pathogenesis through animal models: a mechanism-oriented systems perspective.Frontiers in immunology · 2026Review
- A novel neutralizing antibody recognizing a conserved conformational epitope in PDCoV S1 protein and its therapeutic efficacy in piglets.Journal of virology · 2025Article
- The Different Immune Response Between Onset and Remission of AQP4 Antibody-Positive Optic Neuritis Based on RNA Sequencing of Whole Blood.Journal of inflammation research · 2025Article
- B cell depletion as a therapeutic strategy for neuromyelitis optica spectrum disorder: rationale, evidence, and challenges.Frontiers in immunology · 2025Review
- Autoantibodies in neurological disease.Nature reviews. Immunology · 2021Review
- Induction of Anti-Aquaporin 5 Autoantibody Production by Immunization with a Peptide Derived from the Aquaporin ofImmune network · 2021Article
- Cells to the Rescue: Emerging Cell-Based Treatment Approaches for NMOSD and MOGAD.International journal of molecular sciences · 2021Review
- Pathogenesis of autoimmune demyelination: from multiple sclerosis to neuromyelitis optica spectrum disorders and myelin oligodendrocyte glycoprotein antibody-associated disease.Clinical & translational immunology · 2021Review
Corrections and comments
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Authors and funding
24 authors at 8 institutions in 7 countries.
Funding
Abstract
Most cases of neuromyelitis optica spectrum disorders (NMOSD) harbor pathogenic autoantibodies against the water channel aquaporin 4 (AQP4). Binding of these antibodies to AQP4 on astrocytes initiates damage to these cells, which culminates in the formation of large tissue destructive lesions in the central nervous system (CNS). Consequently, untreated patients may become permanently blind or paralyzed. Studies on the induction and breakage of tolerance to AQP4 could be of great benefit for NMOSD patients. So far, however, all attempts to create suitable animal models by active sensitization have failed. We addressed this challenge and identified peptides, which mimic the conformational AQP4 epitopes recognized by pathogenic antibodies of NMOSD patients. Here we show that these mimotopes can induce the production of AQP4-reactive antibodies in Lewis rats. Hence, our results provide a conceptual framework for the formation of such antibodies in NMOSD patients, and aid to improve immunization strategies for the creation of animal models suitable for tolerance studies in this devastating disease.
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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.