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Figure 5 — Neutrophil-microglia interaction drives motor dysfunction in a neuromyelitis opt
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Created: 2026-04-21T18:29:40
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ID: paper-fig-paper-41665955-5
Figure 5Figure 5
C5ar1 deficiency abrogates downstream microglial activation response to AQP4-IgG infusion. ( A ) Representative confocal images from lumbar cord of wild-type (WT) and C5ar1 -/- mice infused with normal IgG or AQP4-IgG. Lysosomal CD68 immunoreactivity (red) is more abundant in microglia (green) of WT recipients of AQP4-IgG than in C5ar1 –/– recipients. Imaris 3D rendering images illustrate the magnitude of lysosomal expansion. ( B ) ImageJ (NIH) analysis of the percentage area occupied by lysosome inside microglia in the lumbar cord of different experimental groups; treatment: F (1,
20) = 51.35, P < 0.0001; genotype: F (1,
20) = 14.17, P = 0.0066; n = 5–6 mice per group. ( C ) Sholl analysis of microglial branching revealed by Imaris AI-powered filament tracing, which counts the number of microglial filaments intersected by 1 μm spherical steps. Treatment: F (77,
3,730) = 39.35, P < 0.0001; radius: F (3,
95) = 17.02, P < 0.0001; n = 19–32 microglia from
▸Metadata
| pmid | paper-41665955 |
| caption | C5ar1 deficiency abrogates downstream microglial activation response to AQP4-IgG infusion. ( A ) Representative confocal images from lumbar cord of wild-type (WT) and C5ar1 -/- mice infused with no |
| image_url | https://www.ebi.ac.uk/europepmc/articles/PMC13038209/bin/jci-136-199706-g005.jpg |
| paper_title | Neutrophil-microglia interaction drives motor dysfunction in a neuromyelitis optica model induced by subarachnoid AQP4-IgG. |
| figure_label | Figure 5 |
| figure_number | 5 |
| _schema_version | 1 |
| source_strategy | pmc_api |
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