ArticleJCI insight2023
T follicular helper cells contribute to pathophysiology in a model of neuromyelitis optica spectrum disorders.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 14 citations in OpenAlex.
- Microglia and neuroinflammation: function, heterogeneity, and crosstalk.Cellular & molecular immunology · 2026Review
- Distinct remission immune architectures under rituximab and azathioprine in AQP4-IgG-positive neuromyelitis optica spectrum disorder.Frontiers in immunology · 2026Article
- Microglial PD-1/PD-L1 axis in CNS demyelinating diseases: a dual immunoregulatory perspective.Frontiers in cellular neuroscience · 2026Review
- Dissecting NMOSD pathogenesis through animal models: a mechanism-oriented systems perspective.Frontiers in immunology · 2026Review
- CXCL9 associates with experimental neuromyelitis optica spectrum disorder following adoptive transfer of Tfh and Th17 cells.Frontiers in immunology · 2026Article
- Astrocyte-derived extracellular vesicles as antigen-specific therapy for neuromyelitis optica spectrum disorder in the mouse model.bioRxiv : the preprint server for biology · 2025Article
- PPAR-γ activation by pioglitazone inhibits microglia-mediated neuroinflammation and alleviates disease in neuromyelitis optica spectrum disorders.Acta neuropathologica communications · 2025Article
- Cuproptosis Signature Would Reveal the Acute-Remitting Pattern in Patients with Neuromyelitis Optica Spectrum Disorder.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Exercise-mediated IL-6 downstream effects modulate brain pathology-can exercise training protocols influence the downstream effects?Frontiers in neurology · 2025Review
- Outcomes and predictors of relapse and severe pneumonia in Chinese patients with AQP4-IgG-positive neuromyelitis optica spectrum disorder receiving inebilizumab: a prospective cohort study.Frontiers in immunology · 2025Article
- B cell depletion as a therapeutic strategy for neuromyelitis optica spectrum disorder: rationale, evidence, and challenges.Frontiers in immunology · 2025Review
- Effects of intravenous pulse methylprednisolone in neuromyelitis optica during the acute phase.Annals of clinical and translational neurology · 2024Article
- The Role of Gut Microbiota in Neuromyelitis Optica Spectrum Disorder.International journal of molecular sciences · 2024Review
- Correlation of GABABrain and behavior · 2024Article
- Scientific issues with rodent models of neuromyelitis optic spectrum disorders.Frontiers in immunology · 2024Review
- Inhibition of complement C3 signaling ameliorates locomotor and visual dysfunction in autoimmune inflammatory diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Renegade T cell clones and autoimmune disease.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuromyelitis optica spectrum disorders (NMOSD) are inflammatory autoimmune disorders of the CNS. IgG autoantibodies targeting the aquaporin-4 water channel (AQP4-IgGs) are the pathogenic effector of NMOSD. Dysregulated T follicular helper (Tfh) cells have been implicated in loss of B cell tolerance in autoimmune diseases. The contribution of Tfh cells to disease activity and therapeutic potential of targeting these cells in NMOSD remain unclear. Here, we established an autoimmune model of NMOSD by immunizing mice against AQP4 via in vivo electroporation. After AQP4 immunization, mice displayed AQP4 autoantibodies in blood circulation, blood-brain barrier disruption, and IgG infiltration in spinal cord parenchyma. Moreover, AQP4 immunization induced motor impairments and NMOSD-like pathologies, including astrocytopathy, demyelination, axonal loss, and microglia activation. These were associated with increased splenic Tfh, Th1, and Th17 cells; memory B cells; and plasma cells. Aqp4-deficient mice did not display motor impairments and NMOSD-like pathologies after AQP4 immunization. Importantly, abrogating ICOS/ICOS-L signaling using anti-ICOS-L antibody depleted Tfh cells and suppressed the response of Th1 and Th17 cells, memory B cells, and plasma cells in AQP4-immunized mice. These findings were associated with ameliorated motor impairments and spinal cord pathologies. This study suggests a role of Tfh cells in the pathophysiology of NMOSD in a mouse model with AQP4 autoimmunity and provides an animal model for investigating the immunological mechanisms underlying AQP4 autoimmunity and developing therapeutic interventions targeting autoimmune reactions in NMOSD.
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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.