ArticleBrain : a journal of neurology2024
Interferon-γ controls aquaporin 4-specific Th17 and B cells in neuromyelitis optica spectrum disorder.
Article in Brain : a journal of neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The trial behind it
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- B Cells and B Cell Depletion in Autoimmunity and Atherosclerosis.Life (Basel, Switzerland) · 2026Review
- Natural killer cell reduction and dysfunction define a pathogenic and diagnostic axis in neuromyelitis optica spectrum disorder.Journal of neuroinflammation · 2026Article
- Targeted immunomodulation for chronic diseases through advanced delivery platforms.Expert opinion on drug delivery · 2026Review
- Astrocyte-intrinsic signaling of chitinase-like protein CHI3L1 drives inflammation and amplifies demyelination in neuromyelitis optica.The Journal of clinical investigation · 2026Article
- Comparison of clinical and laboratory characteristics of neuromyelitis optica spectrum disorder with or without anti-connective tissue antibodies: an 18-month cohort follow-up.Frontiers in immunology · 2026Article
- Dissecting NMOSD pathogenesis through animal models: a mechanism-oriented systems perspective.Frontiers in immunology · 2026Review
- Astrocyte-derived extracellular vesicles as antigen-specific therapy for neuromyelitis optica spectrum disorder in the mouse model.bioRxiv : the preprint server for biology · 2025Article
- Predict disabling severe attacks in neuromyelitis optica spectrum disorders: warning symptoms and innovative machine learning models.Journal of translational medicine · 2025Article
- Cuproptosis Signature Would Reveal the Acute-Remitting Pattern in Patients with Neuromyelitis Optica Spectrum Disorder.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Type I Interferon Signaling Augments Autoimmunity in Neuromyelitis Optica Spectrum Disorder.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- High-Efficacy Treatment in Neuromyelitis Optica Specturm Disorder Patients With Seropositive AQP4 Antibodies-A Real-World Study.Annals of clinical and translational neurology · 2025Article
- Serum Levels of Aryl Hydrocarbon Receptor Plasma Agonist Activity Are Reduced in Patients With NMOSD and Correlate With Disease Activity.Neurology(R) neuroimmunology & neuroinflammation · 2025Article
- Article
- Peripheral blood immune inflammatory markers in neuromyelitis optica spectrum disorders.Frontiers in neurology · 2025Review
- Engineering neuroimmune regulation: biomaterial and nanotechnology platforms for neuropathology diagnosis and targeted immunomodulation.Frontiers in immunology · 2025Review
- Alterations in peripheral blood immune cell profiles of neuromyelitis optica spectrum disorder across different phases and after B cell depletion therapy.Frontiers in immunology · 2025Article
- Interleukin-6-induced neuroinflammation is exacerbated by subclinical levels of interferon-α.Frontiers in neuroscience · 2025Article
- Therapeutic role of interferon-γ in experimental autoimmune encephalomyelitis is mediated through a tolerogenic subset of splenic CD11bJournal of neuroinflammation · 2024Article
- Association Between Serum Interleukin-32 Level and Disease Status in Cases with Neuromyelitis Optica Spectrum Disorders.Journal of inflammation research · 2024Article
- The levels of circulating cytokines and risk of neuromyelitis optica spectrum disorder: a Mendelian randomization study.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Neuromyelitis optica spectrum disorder (NMOSD) is a CNS autoimmune inflammatory disease mediated by T helper 17 (Th17) and antibody responses to the water channel protein, aquaporin 4 (AQP4), and associated with astrocytopathy, demyelination and axonal loss. Knowledge about disease pathogenesis is limited and the search for new therapies impeded by the absence of a reliable animal model. In our work, we determined that NMOSD is characterized by decreased IFN-γ receptor signalling and that IFN-γ depletion in AQP4201-220-immunized C57BL/6 mice results in severe clinical disease resembling human NMOSD. Pathologically, the disease causes autoimmune astrocytic and CNS injury secondary to cellular and humoral inflammation. Immunologically, the absence of IFN-γ allows for increased expression of IL-6 in B cells and activation of Th17 cells, and generation of a robust autoimmune inflammatory response. Consistent with NMOSD, the experimental disease is exacerbated by administration of IFN-β, whereas repletion of IFN-γ, as well as therapeutic targeting of IL-17A, IL-6R and B cells, ameliorates it. We also demonstrate that immune tolerization with AQP4201-220-coupled poly(lactic-co-glycolic acid) nanoparticles could both prevent and effectively treat the disease. Our findings enhance the understanding of NMOSD pathogenesis and provide a platform for the development of immune tolerance-based therapies, avoiding the limitations of the current immunosuppressive therapies.
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What Socratic holds
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 Socratic graph.