ArticleActa neuropathologica communications2013
T cell-activation in neuromyelitis optica lesions plays a role in their formation.
Article in Acta neuropathologica communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 86 citations in OpenAlex.
- Dissecting NMOSD pathogenesis through animal models: a mechanism-oriented systems perspective.Frontiers in immunology · 2026Review
- AQP4-specific T cells determine lesion localization in the CNS in a model of NMOSD.Acta neuropathologica communications · 2025Article
- Stage-dependent immunity orchestrates AQP4 antibody-guided NMOSD pathology: a role for netting neutrophils with resident memory T cells in situ.Acta neuropathologica · 2024Article
- Interferon-γ controls aquaporin 4-specific Th17 and B cells in neuromyelitis optica spectrum disorder.Brain : a journal of neurology · 2024Article
- Association betweenTranslational neuroscience · 2024Article
- Paths to hippocampal damage in neuromyelitis optica spectrum disorders.Neuropathology and applied neurobiology · 2023Article
- Comparison of OX40 expression in patients with multiple sclerosis and neuromyelitis optica as an approach to diagnosis.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2023Article
- Intruders or protectors - the multifaceted role of B cells in CNS disorders.Frontiers in cellular neuroscience · 2023Review
- Delimiting MOGAD as a disease entity using translational imaging.Frontiers in neurology · 2023Review
- Trifluoperazine reduces apoptosis and inflammatory responses in traumatic brain injury by preventing the accumulation of Aquaporin4 on the surface of brain cells.International journal of medical sciences · 2023Article
- Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease.Frontiers in neurology · 2023Review
- P2R Inhibitors Prevent Antibody-Mediated Complement Activation in an Animal Model of Neuromyelitis Optica : P2R Inhibitors Prevent Autoantibody Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- 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
- Hope for patients with neuromyelitis optica spectrum disorders - from mechanisms to trials.Nature reviews. Neurology · 2021Review
- Regulatory T cells protect against brain damage by alleviating inflammatory response in neuromyelitis optica spectrum disorder.Journal of neuroinflammation · 2021Article
- In vivo NIR-II structured-illumination light-sheet microscopy.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- New Therapeutic Landscape in Neuromyelitis Optica.Current treatment options in neurology · 2021Review
- The Emerging Role of Microglia in Neuromyelitis Optica.Frontiers in immunology · 2021Review
- Induction of aquaporin 4-reactive antibodies in Lewis rats immunized with aquaporin 4 mimotopes.Acta neuropathologica communications · 2020Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 4 countries.
Funding
Abstract
backgroundNeuromyelitis optica (NMO) is an inflammatory demyelinating disease of the central nervous system (CNS), which is characterized by the presence of pathogenic serum autoantibodies against aquaporin 4 (AQP4) in the vast majority of patients. The contribution of T cells to the formation of astrocyte destructive lesions is currently unclear. However, active human NMO lesions contain CD4+ T-lymphocytes expressing the activation marker Ox40, and the expression is more profound compared to that seen in MS lesions of comparable activity. Therefore, we analyzed the role of T-cell activation within the CNS in the initiation of NMO lesions in an experimental model of co-transfer of different encephalitogenic T-cells and human AQP4 antibody containing NMO immunoglobulin (NMO IgG). We further studied the expression of the T-cell activation marker Ox40 in NMO and multiple sclerosis lesions in different stages of activity.
resultsAll encephalitogenic T-cell lines used in our experiments induced brain inflammation with a comparable extent of blood brain barrier damage, allowing human NMO IgG to penetrate into the brain and spinal cord tissue. However, astrocyte destructive NMO lesions were only seen with T-cells, which showed signs of activation in the lesions. T-cell activation was reflected by the expression of the activation marker Ox40 and pronounced production of γ-IFN, which was able to increase the production of complement proteins and of the Fc gamma III receptor (Fcgr3) and decreased production of complement inhibitory protein Factor H in microglia.
conclusionsOur data indicate that local activation of T-cells provide an inflammatory environment in the CNS, which allows AQP4 auto-antibodies to induce astrocyte destructive NMO-like lesions.
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