ArticleActa neuropathologica2015
Highly encephalitogenic aquaporin 4-specific T cells and NMO-IgG jointly orchestrate lesion location and tissue damage in the CNS.
Article in Acta neuropathologica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
What it found
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Who cites it
51 citing papers in PubMed, 72 citations in OpenAlex.
- Dynamic characterization of pathological and functional deterioration in a mouse model of optic neuritis related to neuromyelitis optica spectrum disorder.Neural regeneration research · 2026Article
- Progress on experimental models of neuromyelitis optica spectrum disease.IBRO neuroscience reports · 2026Review
- Causal Exposures of Immune Cells in Neuromyelitis Optica Spectrum Disorders: A Mendelian Randomization Study and Flow Cytometry Analysis.Brain and behavior · 2026Article
- Dissecting NMOSD pathogenesis through animal models: a mechanism-oriented systems perspective.Frontiers in immunology · 2026Review
- CD4-Positive T-Cell Responses to MOG Peptides in MOG Antibody-Associated Disease.International journal of molecular sciences · 2025Article
- AQP4-specific T cells determine lesion localization in the CNS in a model of NMOSD.Acta neuropathologica communications · 2025Article
- Linking Downbeat Nystagmus and Aquaporin-4-Positive Neuromyelitis Optica: A Closer Look at Their Hidden Relationship.Cureus · 2024Article
- Humanized-Aquaporin-4-Expressing Rat Created by Gene-Editing Technology and Its Use to Clarify the Pathology of Neuromyelitis Optica Spectrum Disorder.International journal of molecular sciences · 2024Article
- Scientific issues with rodent models of neuromyelitis optic spectrum disorders.Frontiers in immunology · 2024Review
- Immune Repertoire Profiling Reveals Its Clinical Application Potential and Triggers for Neuromyelitis Optica Spectrum Disorders.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
- Paths to hippocampal damage in neuromyelitis optica spectrum disorders.Neuropathology and applied neurobiology · 2023Article
- In utero exposure to maternal anti-aquaporin-4 antibodies alters brain vasculature and neural dynamics in male mouse offspring.Science translational medicine · 2022Article
- Rare variants and HLA haplotypes associated in patients with 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
- Hypothalamic lesions in neuromyelitis optica spectrum disorders: exploring a scoring system based on magnetic resonance imaging.Japanese journal of radiology · 2021Article
- Matrine treatment reduces retinal ganglion cell apoptosis in experimental optic neuritis.Scientific reports · 2021Article
- CNS autoimmunity in children: An unwanted wrinkle in a smooth narrative.Medical journal, Armed Forces India · 2021Review
- CD8Annals of clinical and translational neurology · 2021Article
Corrections and comments
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Authors and funding
17 authors at 8 institutions in 4 countries.
Funding
Abstract
In neuromyelitis optica (NMO), astrocytes become targets for pathogenic aquaporin 4 (AQP4)-specific antibodies which gain access to the central nervous system (CNS) in the course of inflammatory processes. Since these antibodies belong to a T cell-dependent subgroup of immunoglobulins, and since NMO lesions contain activated CD4(+) T cells, the question arose whether AQP4-specific T cells might not only provide T cell help for antibody production, but also play an important role in the induction of NMO lesions. We show here that highly pathogenic, AQP4-peptide-specific T cells exist in Lewis rats, which recognize AQP4268-285 as their specific antigen and cause severe panencephalitis. These T cells are re-activated behind the blood-brain barrier and deeply infiltrate the CNS parenchyma of the optic nerves, the brain, and the spinal cord, while T cells with other AQP4-peptide specificities are essentially confined to the meninges. Although AQP4268-285-specific T cells are found throughout the entire neuraxis, they have NMO-typical "hotspots" for infiltration, i.e. periventricular and periaqueductal regions, hypothalamus, medulla, the dorsal horns of spinal cord, and the optic nerves. Most remarkably, together with NMO-IgG, they initiate large astrocyte-destructive lesions which are located predominantly in spinal cord gray matter. We conclude that the processing of AQP4 by antigen presenting cells in Lewis rats produces a highly encephalitogenic AQP4 epitope (AQP4268-285), that T cells specific for this epitope are found in the immune repertoire of normal Lewis rats and can be readily expanded, and that AQP4268-285-specific T cells produce NMO-like lesions in the presence of NMO-IgG.
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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.