ArticleGlia2025
Distinguishing Neuromyelitis Optica Spectrum Disorders Subtypes: A Study on AQP4 and C3d Epitope Expression in Cytokine-Primed Human Astrocytes.
Article in Glia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Astrocyte-derived extracellular vesicles as antigen-specific therapy for neuromyelitis optica spectrum disorder in the mouse model.bioRxiv : the preprint server for biology · 2025Article
- Serum Aquaporin-4 Antibody Status and TGF-β in Neuromyelitis Optica Spectrum Disorder: Impact on Astrocyte Function and Correlation with Disease Activity and Severity.Neurology international · 2025Article
- SARS-CoV-2 Spike Protein and Molecular Mimicry: An Immunoinformatic Screen for Cross-Reactive Autoantigen Candidates.International journal of molecular sciences · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
Neuromyelitis optica spectrum disorders (NMOSD) are severe autoimmune conditions affecting the central nervous system. In a subset of cases, no autoantibodies are detectable with the currently used routine assays. This study aimed to determine whether the levels of expression of aquaporin-4 (AQP4), excitatory amino acid transporter 2 (EAAT2), or complement C3/C3d and C5b-9 in human astrocytes following incubation with patient sera under inflammatory conditions differ between the various NMOSD subtypes and whether such differences can help to identify autoantibody-mediated cases of NMOSD. Levels of AQP4, EAAT2, complement C3/C3d and C5b-9 epitope expression on human astrocytes pretreated with various cytokines were quantitatively analyzed via indirect immunofluorescence after exposure to sera from patients with AQP4-IgG seropositive, MOG-IgG seropositive, and AQP4/MOG-IgG double seronegative NMOSD. Significant differences in AQP4 and C3d epitope expression were observed, with IL-17A, IL-10, and IL-6 pre-treatment notably influencing astrocytic responses. Using uniform manifold approximation and projection (UMAP), patients were classified into clusters corresponding to AQP4-IgG seropositive, MOG-IgG seropositive, or double seronegative NMOSD. These results demonstrate distinct astrocytic staining patterns across NMOSD subtypes, providing a potential diagnostic tool for distinguishing between autoantibody-mediated astrocytopathy and other cases. These findings suggest specific pathogenic mechanisms linked to each NMOSD subtype, which may have implications for tailoring therapeutic strategies based on cytokine involvement and astrocyte reactivity.
Indexed as
Identifiers
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.