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Figure 7 — 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-41665955-7
Figure 7Figure 7
Microglia are required for pathogenic AQP4-IgG to upregulate CXCL1 in cultured mouse astrocytes. ( A ) Experimental design of the IgG binding to AQP4 on astrocytes in primary glial cultures established from wild-type and Aqp4 –/– pup brains. Microglia were depleted by treating Clodrosome (100 μg/mL) before subculture. Two days after adding IgG or cytokines, CXCL1 production was assessed by immunostaining or ELISA. ( B ) Immunoblot analysis of WT, Aqp4 –/– primary glial cells using IgGs specific for AQP4 and actin (loading control). ( C ) CXCL1 immunoreactivity was assessed in wild-type and AQP4 ± cells exposed to a control nonpathogenic monoclonal mouse IgG specific for the AQP4 cytoplasmic C-terminal domain (CCD-AQP4-IgG, m5) or a pathogenic extracellular domain–reactive IgG (ECD-AQP4-IgG, m21) or to IFN-γ plus TNF-α cytokines. Astrocytes are identified by AQP4 and GFAP immunoreactivities; microglia by IBA1; DNA is blue (DAPI). ( D ) Cellular CXCL1 (upper) was quantified from flu
▸Metadata
| pmid | paper-41665955 |
| caption | Microglia are required for pathogenic AQP4-IgG to upregulate CXCL1 in cultured mouse astrocytes. ( A ) Experimental design of the IgG binding to AQP4 on astrocytes in primary glial cultures establishe |
| image_url | https://www.ebi.ac.uk/europepmc/articles/PMC13038209/bin/jci-136-199706-g007.jpg |
| paper_title | Neutrophil-microglia interaction drives motor dysfunction in a neuromyelitis optica model induced by subarachnoid AQP4-IgG. |
| figure_label | Figure 7 |
| figure_number | 7 |
| _schema_version | 1 |
| source_strategy | pmc_api |
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