ArticleActa neuropathologica communications2015
Pathogenic aquaporin-4 reactive T cells are sufficient to induce mouse model of neuromyelitis optica.
Article in Acta neuropathologica communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 54 citations in OpenAlex.
- Progress on experimental models of neuromyelitis optica spectrum disease.IBRO neuroscience reports · 2026Review
- CXCL9 associates with experimental neuromyelitis optica spectrum disorder following adoptive transfer of Tfh and Th17 cells.Frontiers in immunology · 2026Article
- Sjögren Syndrome Candidate Autoantigen AQP5 Triggers AQP4 CNS Autoimmunity Through Self-Antigen Mimicry.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- Dissecting NMOSD pathogenesis through animal models: a mechanism-oriented systems perspective.Frontiers in immunology · 2026Review
- Type I Interferon Signaling Augments Autoimmunity in Neuromyelitis Optica Spectrum Disorder.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- AQP4-specific T cells determine lesion localization in the CNS in a model of NMOSD.Acta neuropathologica communications · 2025Article
- Modeling MOG Antibody-Associated Disorder and Neuromyelitis Optica Spectrum Disorder in Animal Models: Visual System Manifestations.Neurology(R) neuroimmunology & neuroinflammation · 2023Article
- T cell deletional tolerance restricts AQP4 but not MOG CNS autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Granzyme B in circulating CD8+ T cells as a biomarker of immunotherapy effectiveness and disability in neuromyelitis optica spectrum disorders.Frontiers in immunology · 2022Article
- Targeting the complement system in neuromyelitis optica spectrum disorder.Expert opinion on biological therapy · 2021Review
- Cells to the Rescue: Emerging Cell-Based Treatment Approaches for NMOSD and MOGAD.International journal of molecular sciences · 2021Review
- CNS autoimmunity in children: An unwanted wrinkle in a smooth narrative.Medical journal, Armed Forces India · 2021Review
- Low Frequency Ultrasound With Injection of NMO-IgG and Complement Produces Lesions Different From Experimental Autoimmune Encephalomyelitis Mice.Frontiers in immunology · 2021Article
- The Emerging Role of Microglia in Neuromyelitis Optica.Frontiers in immunology · 2021Review
- Lower serum interleukin-22 and interleukin-35 levels are associated with disease status in neuromyelitis optica spectrum disorders.CNS neuroscience & therapeutics · 2020Article
- Comparative Analysis of T-Cell Responses to Aquaporin-4 and Myelin Oligodendrocyte Glycoprotein in Inflammatory Demyelinating Central Nervous System Diseases.Frontiers in immunology · 2020Article
- Experimental animal models of aquaporin-4-IgG-seropositive neuromyelitis optica spectrum disorders: progress and shortcomings.Brain pathology (Zurich, Switzerland) · 2020Review
- Rodent Models of Optic Neuritis.Frontiers in neurology · 2020Review
- Review
- NMO-IgG and AQP4 Peptide Can Induce Aggravation of EAMG and Immune-Mediated Muscle Weakness.Journal of immunology research · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
introductionNeuromyelitis Optica (NMO) is an autoimmune disease primarily targeting the spinal cord and optic nerve leading to paralysis and blindness. The discovery of an antibody against the astrocytic water channel, aquaporin-4 (AQP4), in the majority of patients, has led to the presumption that the antibody was necessary for disease pathogenesis. The potential role of T cells in the central nervous system, however, has not been thoroughly examined.
resultsWe generated an anti-AQP4 antibody seronegative model of NMO using pathogenic AQP4-reactive T cells in mice by immunizing AQP4 null mice with peptides corresponding to the second extracellular loop of AQP4, loop C. When polarized to a Th17 phenotype and transferred to wild-type mice, these cells caused tail and limb weakness. Histology showed demyelination and T cell infiltration in the spinal cord, optic nerve and brain. Animals receiving cells re-stimulated in culture with non-specific proteins resulted in no behavioral disease, indicating that specific targeting of AQP4 is essential for this phenotype.
conclusionsIn summary, we show that AQP4-reactive T cells are sufficient to trigger an NMO-like disease in mice, independent of antibodies, indicating that pathogenic AQP4-reactive T cells may play a similar role in humans.
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