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anti mouse il  (R&D Systems)


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    R&D Systems anti mouse il
    IL-25 activates ILC2s and stimulates the production of downstream factors <t>IL-5/IL-13.</t> A Single-Cell transcriptomic atlas of after TBI mice brain UMAP projection of 29,046 single cells isolated from cerebral cortex tissues of Sham (7,963), TBI + PBS (9,332 ), and TBI + IL-25 (11,751) groups. Colors represent distinct cell populations identified through unsupervised clustering. B Proportions of BBB-associated cells (endothelial cells, astrocytes, pericytes) across Sham, TBI + PBS, and TBI + IL-25 groups. C Heatmap visualization of differentially expressed genes in endothelial cells isolated from Sham, TBI + PBS, and TBI + IL-25 treatment groups. D KEGG network pathway enrichment analysis of differentially expressed genes in endothelial cells from the SHAM, TBI + PBS, and TBI + IL-25 groups. E Integrated KEGG pathway analysis of the three groups. F Cell-cell communication analysis depicting differential gene expression between endothelial cells and ILC2s. G Flow cytometry gating strategy for ILC2 identification: lymphocytes were selected by FSC/SSC, followed by detection of Lin - CD45 + CD127 + ST2 + cells. H - I Representative flow plots ( H ) and quantitative analysis ( I ) of cerebral cortex ILC2s at 3 days after TBI ( n = 3 per group). J - M Cytokine levels in ipsilateral cerebral cortex tissue and serum at 3 days after TBI: IL-5 (cerebral cortex) ( J ), IL-5 (serum) ( K ), IL-13 (cerebral cortex) ( L ), IL-13 (serum) ( M ) ( n = 6 per group). Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
    Anti Mouse Il, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 23 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "IL-25–ILC2–IL-13 axis improves traumatic brain injury by mediating CXCL-10-dependent regulation of blood brain barrier integrity"

    Article Title: IL-25–ILC2–IL-13 axis improves traumatic brain injury by mediating CXCL-10-dependent regulation of blood brain barrier integrity

    Journal: Journal of Neuroinflammation

    doi: 10.1186/s12974-026-03696-4

    IL-25 activates ILC2s and stimulates the production of downstream factors IL-5/IL-13. A Single-Cell transcriptomic atlas of after TBI mice brain UMAP projection of 29,046 single cells isolated from cerebral cortex tissues of Sham (7,963), TBI + PBS (9,332 ), and TBI + IL-25 (11,751) groups. Colors represent distinct cell populations identified through unsupervised clustering. B Proportions of BBB-associated cells (endothelial cells, astrocytes, pericytes) across Sham, TBI + PBS, and TBI + IL-25 groups. C Heatmap visualization of differentially expressed genes in endothelial cells isolated from Sham, TBI + PBS, and TBI + IL-25 treatment groups. D KEGG network pathway enrichment analysis of differentially expressed genes in endothelial cells from the SHAM, TBI + PBS, and TBI + IL-25 groups. E Integrated KEGG pathway analysis of the three groups. F Cell-cell communication analysis depicting differential gene expression between endothelial cells and ILC2s. G Flow cytometry gating strategy for ILC2 identification: lymphocytes were selected by FSC/SSC, followed by detection of Lin - CD45 + CD127 + ST2 + cells. H - I Representative flow plots ( H ) and quantitative analysis ( I ) of cerebral cortex ILC2s at 3 days after TBI ( n = 3 per group). J - M Cytokine levels in ipsilateral cerebral cortex tissue and serum at 3 days after TBI: IL-5 (cerebral cortex) ( J ), IL-5 (serum) ( K ), IL-13 (cerebral cortex) ( L ), IL-13 (serum) ( M ) ( n = 6 per group). Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
    Figure Legend Snippet: IL-25 activates ILC2s and stimulates the production of downstream factors IL-5/IL-13. A Single-Cell transcriptomic atlas of after TBI mice brain UMAP projection of 29,046 single cells isolated from cerebral cortex tissues of Sham (7,963), TBI + PBS (9,332 ), and TBI + IL-25 (11,751) groups. Colors represent distinct cell populations identified through unsupervised clustering. B Proportions of BBB-associated cells (endothelial cells, astrocytes, pericytes) across Sham, TBI + PBS, and TBI + IL-25 groups. C Heatmap visualization of differentially expressed genes in endothelial cells isolated from Sham, TBI + PBS, and TBI + IL-25 treatment groups. D KEGG network pathway enrichment analysis of differentially expressed genes in endothelial cells from the SHAM, TBI + PBS, and TBI + IL-25 groups. E Integrated KEGG pathway analysis of the three groups. F Cell-cell communication analysis depicting differential gene expression between endothelial cells and ILC2s. G Flow cytometry gating strategy for ILC2 identification: lymphocytes were selected by FSC/SSC, followed by detection of Lin - CD45 + CD127 + ST2 + cells. H - I Representative flow plots ( H ) and quantitative analysis ( I ) of cerebral cortex ILC2s at 3 days after TBI ( n = 3 per group). J - M Cytokine levels in ipsilateral cerebral cortex tissue and serum at 3 days after TBI: IL-5 (cerebral cortex) ( J ), IL-5 (serum) ( K ), IL-13 (cerebral cortex) ( L ), IL-13 (serum) ( M ) ( n = 6 per group). Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Techniques Used: Single Cell, Isolation, Gene Expression, Flow Cytometry

    IL-13 preserves BBB integrity and attenuates pyroptosis in bEnd.3 cells after OGD/R injury. A Experimental workflow of OGD/R modeling and treatment in bEnd.3 cells. (B-C) IL-5 ( B ) and IL-13 ( C ) levels in supernatants of bEnd.3 cells after OGD/R ± IL-25 treatment (n = 6 per group). D - H Western blot analysis of bEnd.3 cells after OGD/R with or without IL-25, IL-5, or IL-13 treatment: Representative blots ( D ), ZO-1 quantification ( E ), Occludin quantification ( F ), Claudin-5 quantification ( G ), Caspase-1 quantification ( H ) (n = 6 per group). I - J Representative flow cytometry plots ( I ) and quantitative analysis ( J ) of apoptosis in bEnd.3 cells subjected to OGD/R with or without IL-25, IL-5, or IL-13 treatment (n = 6 per group). Viable cells: Annexin V⁻/PI⁻; Early apoptotic: Annexin V⁺/PI⁻; Late apoptotic: Annexin V⁺/PI⁺. K Immunofluorescence of ZO-1 and Claudin-5 (green) in bEnd.3 cells monolayers after OGD/R ± IL-13 treatment. Nuclei counterstained with DAPI (blue). Scale bar = 100 μm. Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
    Figure Legend Snippet: IL-13 preserves BBB integrity and attenuates pyroptosis in bEnd.3 cells after OGD/R injury. A Experimental workflow of OGD/R modeling and treatment in bEnd.3 cells. (B-C) IL-5 ( B ) and IL-13 ( C ) levels in supernatants of bEnd.3 cells after OGD/R ± IL-25 treatment (n = 6 per group). D - H Western blot analysis of bEnd.3 cells after OGD/R with or without IL-25, IL-5, or IL-13 treatment: Representative blots ( D ), ZO-1 quantification ( E ), Occludin quantification ( F ), Claudin-5 quantification ( G ), Caspase-1 quantification ( H ) (n = 6 per group). I - J Representative flow cytometry plots ( I ) and quantitative analysis ( J ) of apoptosis in bEnd.3 cells subjected to OGD/R with or without IL-25, IL-5, or IL-13 treatment (n = 6 per group). Viable cells: Annexin V⁻/PI⁻; Early apoptotic: Annexin V⁺/PI⁻; Late apoptotic: Annexin V⁺/PI⁺. K Immunofluorescence of ZO-1 and Claudin-5 (green) in bEnd.3 cells monolayers after OGD/R ± IL-13 treatment. Nuclei counterstained with DAPI (blue). Scale bar = 100 μm. Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Techniques Used: Western Blot, Flow Cytometry, Immunofluorescence

    IL-13 improves BBB function by reducing CXCL-10 expression. A - B Cytokine array analysis identified CXCL-10 as one of the significantly downregulated cytokines in the IL-13-treated groups ( n = 3 per group). C - D CXCL-10 expression in bEnd.3 cells subjected to OGD/R ± IL-25, IL-5, or IL-13: Representative Western blot ( C ) and quantification ( D ) ( n = 6 per group). E - F CXCL-10 levels in ipsilateral cortex 3 days after TBI: Representative blot ( E ) and quantification ( F ) ( n = 6 per group). G Experimental workflow of TBI modeling and therapeutic administration. H - K Western blot analysis of TJs (ZO-1, Occludin, Claudin-5) in the ipsilateral cortex 3 days after TBI: Representative blots ( H ), ZO-1 quantification ( I ), Occludin quantification ( J ), Claudin-5 quantification ( K ) ( n = 6 per group). Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
    Figure Legend Snippet: IL-13 improves BBB function by reducing CXCL-10 expression. A - B Cytokine array analysis identified CXCL-10 as one of the significantly downregulated cytokines in the IL-13-treated groups ( n = 3 per group). C - D CXCL-10 expression in bEnd.3 cells subjected to OGD/R ± IL-25, IL-5, or IL-13: Representative Western blot ( C ) and quantification ( D ) ( n = 6 per group). E - F CXCL-10 levels in ipsilateral cortex 3 days after TBI: Representative blot ( E ) and quantification ( F ) ( n = 6 per group). G Experimental workflow of TBI modeling and therapeutic administration. H - K Western blot analysis of TJs (ZO-1, Occludin, Claudin-5) in the ipsilateral cortex 3 days after TBI: Representative blots ( H ), ZO-1 quantification ( I ), Occludin quantification ( J ), Claudin-5 quantification ( K ) ( n = 6 per group). Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Techniques Used: Expressing, Western Blot

    IL-13 improves BBB function by reducing CXCL-10 expression. A - D Western blot analysis of TJs (ZO-1, Occludin, Claudin-5) in the ipsilateral cortex 3 days after TBI: Representative blots ( A ), ZO-1 quantification ( B ), Occludin quantification ( C ), Claudin-5 quantification ( D ) ( n = 6 per group). E Immunofluorescence of ZO-1 (red) co-stained with CD31 (endothelial cells) (green) in the ipsilateral cortex 3 days after TBI. Nuclei were counterstained with DAPI (blue). Scale bar = 50 μm. F Immunofluorescence of TUNEL (green) co-stained with CD31 (endothelial cells) (red) in the ipsilateral cortex 3 days after TBI. Nuclei were counterstained with DAPI (blue). Scale bar = 20 μm. G Quantification of endothelial expression of ZO-1 in the ipsilateral cortex 3 days after TBI ( n = 6 per group). H Quantification of endothelial expression of TUNEL in the ipsilateral cortex 3 days after TBI ( n = 6 per group). I Representative macroscopic images of Evans Blue extravasation (blue areas) in brain tissue 3 days after TBI. J Quantitative analysis of Evans Blue leakage in ipsilateral hemispheres ( n = 6 per group). Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
    Figure Legend Snippet: IL-13 improves BBB function by reducing CXCL-10 expression. A - D Western blot analysis of TJs (ZO-1, Occludin, Claudin-5) in the ipsilateral cortex 3 days after TBI: Representative blots ( A ), ZO-1 quantification ( B ), Occludin quantification ( C ), Claudin-5 quantification ( D ) ( n = 6 per group). E Immunofluorescence of ZO-1 (red) co-stained with CD31 (endothelial cells) (green) in the ipsilateral cortex 3 days after TBI. Nuclei were counterstained with DAPI (blue). Scale bar = 50 μm. F Immunofluorescence of TUNEL (green) co-stained with CD31 (endothelial cells) (red) in the ipsilateral cortex 3 days after TBI. Nuclei were counterstained with DAPI (blue). Scale bar = 20 μm. G Quantification of endothelial expression of ZO-1 in the ipsilateral cortex 3 days after TBI ( n = 6 per group). H Quantification of endothelial expression of TUNEL in the ipsilateral cortex 3 days after TBI ( n = 6 per group). I Representative macroscopic images of Evans Blue extravasation (blue areas) in brain tissue 3 days after TBI. J Quantitative analysis of Evans Blue leakage in ipsilateral hemispheres ( n = 6 per group). Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Techniques Used: Expressing, Western Blot, Immunofluorescence, Staining, TUNEL Assay

    Graphical abstract: IL-25-activated ILC2s secrete IL-13 to improve BBB function after TBI, by Figdraw
    Figure Legend Snippet: Graphical abstract: IL-25-activated ILC2s secrete IL-13 to improve BBB function after TBI, by Figdraw

    Techniques Used:



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    Image Search Results


    IL-25 activates ILC2s and stimulates the production of downstream factors IL-5/IL-13. A Single-Cell transcriptomic atlas of after TBI mice brain UMAP projection of 29,046 single cells isolated from cerebral cortex tissues of Sham (7,963), TBI + PBS (9,332 ), and TBI + IL-25 (11,751) groups. Colors represent distinct cell populations identified through unsupervised clustering. B Proportions of BBB-associated cells (endothelial cells, astrocytes, pericytes) across Sham, TBI + PBS, and TBI + IL-25 groups. C Heatmap visualization of differentially expressed genes in endothelial cells isolated from Sham, TBI + PBS, and TBI + IL-25 treatment groups. D KEGG network pathway enrichment analysis of differentially expressed genes in endothelial cells from the SHAM, TBI + PBS, and TBI + IL-25 groups. E Integrated KEGG pathway analysis of the three groups. F Cell-cell communication analysis depicting differential gene expression between endothelial cells and ILC2s. G Flow cytometry gating strategy for ILC2 identification: lymphocytes were selected by FSC/SSC, followed by detection of Lin - CD45 + CD127 + ST2 + cells. H - I Representative flow plots ( H ) and quantitative analysis ( I ) of cerebral cortex ILC2s at 3 days after TBI ( n = 3 per group). J - M Cytokine levels in ipsilateral cerebral cortex tissue and serum at 3 days after TBI: IL-5 (cerebral cortex) ( J ), IL-5 (serum) ( K ), IL-13 (cerebral cortex) ( L ), IL-13 (serum) ( M ) ( n = 6 per group). Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Journal: Journal of Neuroinflammation

    Article Title: IL-25–ILC2–IL-13 axis improves traumatic brain injury by mediating CXCL-10-dependent regulation of blood brain barrier integrity

    doi: 10.1186/s12974-026-03696-4

    Figure Lengend Snippet: IL-25 activates ILC2s and stimulates the production of downstream factors IL-5/IL-13. A Single-Cell transcriptomic atlas of after TBI mice brain UMAP projection of 29,046 single cells isolated from cerebral cortex tissues of Sham (7,963), TBI + PBS (9,332 ), and TBI + IL-25 (11,751) groups. Colors represent distinct cell populations identified through unsupervised clustering. B Proportions of BBB-associated cells (endothelial cells, astrocytes, pericytes) across Sham, TBI + PBS, and TBI + IL-25 groups. C Heatmap visualization of differentially expressed genes in endothelial cells isolated from Sham, TBI + PBS, and TBI + IL-25 treatment groups. D KEGG network pathway enrichment analysis of differentially expressed genes in endothelial cells from the SHAM, TBI + PBS, and TBI + IL-25 groups. E Integrated KEGG pathway analysis of the three groups. F Cell-cell communication analysis depicting differential gene expression between endothelial cells and ILC2s. G Flow cytometry gating strategy for ILC2 identification: lymphocytes were selected by FSC/SSC, followed by detection of Lin - CD45 + CD127 + ST2 + cells. H - I Representative flow plots ( H ) and quantitative analysis ( I ) of cerebral cortex ILC2s at 3 days after TBI ( n = 3 per group). J - M Cytokine levels in ipsilateral cerebral cortex tissue and serum at 3 days after TBI: IL-5 (cerebral cortex) ( J ), IL-5 (serum) ( K ), IL-13 (cerebral cortex) ( L ), IL-13 (serum) ( M ) ( n = 6 per group). Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Article Snippet: An anti-mouse IL-13 neutralizing antibody (MAB413, R&D SYSTEMS, USA) was administered via i.p. injection at a dose of 100 μg per mouse 1 day before TBI, followed by daily injections for two consecutive days [ ].

    Techniques: Single Cell, Isolation, Gene Expression, Flow Cytometry

    IL-13 preserves BBB integrity and attenuates pyroptosis in bEnd.3 cells after OGD/R injury. A Experimental workflow of OGD/R modeling and treatment in bEnd.3 cells. (B-C) IL-5 ( B ) and IL-13 ( C ) levels in supernatants of bEnd.3 cells after OGD/R ± IL-25 treatment (n = 6 per group). D - H Western blot analysis of bEnd.3 cells after OGD/R with or without IL-25, IL-5, or IL-13 treatment: Representative blots ( D ), ZO-1 quantification ( E ), Occludin quantification ( F ), Claudin-5 quantification ( G ), Caspase-1 quantification ( H ) (n = 6 per group). I - J Representative flow cytometry plots ( I ) and quantitative analysis ( J ) of apoptosis in bEnd.3 cells subjected to OGD/R with or without IL-25, IL-5, or IL-13 treatment (n = 6 per group). Viable cells: Annexin V⁻/PI⁻; Early apoptotic: Annexin V⁺/PI⁻; Late apoptotic: Annexin V⁺/PI⁺. K Immunofluorescence of ZO-1 and Claudin-5 (green) in bEnd.3 cells monolayers after OGD/R ± IL-13 treatment. Nuclei counterstained with DAPI (blue). Scale bar = 100 μm. Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Journal: Journal of Neuroinflammation

    Article Title: IL-25–ILC2–IL-13 axis improves traumatic brain injury by mediating CXCL-10-dependent regulation of blood brain barrier integrity

    doi: 10.1186/s12974-026-03696-4

    Figure Lengend Snippet: IL-13 preserves BBB integrity and attenuates pyroptosis in bEnd.3 cells after OGD/R injury. A Experimental workflow of OGD/R modeling and treatment in bEnd.3 cells. (B-C) IL-5 ( B ) and IL-13 ( C ) levels in supernatants of bEnd.3 cells after OGD/R ± IL-25 treatment (n = 6 per group). D - H Western blot analysis of bEnd.3 cells after OGD/R with or without IL-25, IL-5, or IL-13 treatment: Representative blots ( D ), ZO-1 quantification ( E ), Occludin quantification ( F ), Claudin-5 quantification ( G ), Caspase-1 quantification ( H ) (n = 6 per group). I - J Representative flow cytometry plots ( I ) and quantitative analysis ( J ) of apoptosis in bEnd.3 cells subjected to OGD/R with or without IL-25, IL-5, or IL-13 treatment (n = 6 per group). Viable cells: Annexin V⁻/PI⁻; Early apoptotic: Annexin V⁺/PI⁻; Late apoptotic: Annexin V⁺/PI⁺. K Immunofluorescence of ZO-1 and Claudin-5 (green) in bEnd.3 cells monolayers after OGD/R ± IL-13 treatment. Nuclei counterstained with DAPI (blue). Scale bar = 100 μm. Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Article Snippet: An anti-mouse IL-13 neutralizing antibody (MAB413, R&D SYSTEMS, USA) was administered via i.p. injection at a dose of 100 μg per mouse 1 day before TBI, followed by daily injections for two consecutive days [ ].

    Techniques: Western Blot, Flow Cytometry, Immunofluorescence

    IL-13 improves BBB function by reducing CXCL-10 expression. A - B Cytokine array analysis identified CXCL-10 as one of the significantly downregulated cytokines in the IL-13-treated groups ( n = 3 per group). C - D CXCL-10 expression in bEnd.3 cells subjected to OGD/R ± IL-25, IL-5, or IL-13: Representative Western blot ( C ) and quantification ( D ) ( n = 6 per group). E - F CXCL-10 levels in ipsilateral cortex 3 days after TBI: Representative blot ( E ) and quantification ( F ) ( n = 6 per group). G Experimental workflow of TBI modeling and therapeutic administration. H - K Western blot analysis of TJs (ZO-1, Occludin, Claudin-5) in the ipsilateral cortex 3 days after TBI: Representative blots ( H ), ZO-1 quantification ( I ), Occludin quantification ( J ), Claudin-5 quantification ( K ) ( n = 6 per group). Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Journal: Journal of Neuroinflammation

    Article Title: IL-25–ILC2–IL-13 axis improves traumatic brain injury by mediating CXCL-10-dependent regulation of blood brain barrier integrity

    doi: 10.1186/s12974-026-03696-4

    Figure Lengend Snippet: IL-13 improves BBB function by reducing CXCL-10 expression. A - B Cytokine array analysis identified CXCL-10 as one of the significantly downregulated cytokines in the IL-13-treated groups ( n = 3 per group). C - D CXCL-10 expression in bEnd.3 cells subjected to OGD/R ± IL-25, IL-5, or IL-13: Representative Western blot ( C ) and quantification ( D ) ( n = 6 per group). E - F CXCL-10 levels in ipsilateral cortex 3 days after TBI: Representative blot ( E ) and quantification ( F ) ( n = 6 per group). G Experimental workflow of TBI modeling and therapeutic administration. H - K Western blot analysis of TJs (ZO-1, Occludin, Claudin-5) in the ipsilateral cortex 3 days after TBI: Representative blots ( H ), ZO-1 quantification ( I ), Occludin quantification ( J ), Claudin-5 quantification ( K ) ( n = 6 per group). Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Article Snippet: An anti-mouse IL-13 neutralizing antibody (MAB413, R&D SYSTEMS, USA) was administered via i.p. injection at a dose of 100 μg per mouse 1 day before TBI, followed by daily injections for two consecutive days [ ].

    Techniques: Expressing, Western Blot

    IL-13 improves BBB function by reducing CXCL-10 expression. A - D Western blot analysis of TJs (ZO-1, Occludin, Claudin-5) in the ipsilateral cortex 3 days after TBI: Representative blots ( A ), ZO-1 quantification ( B ), Occludin quantification ( C ), Claudin-5 quantification ( D ) ( n = 6 per group). E Immunofluorescence of ZO-1 (red) co-stained with CD31 (endothelial cells) (green) in the ipsilateral cortex 3 days after TBI. Nuclei were counterstained with DAPI (blue). Scale bar = 50 μm. F Immunofluorescence of TUNEL (green) co-stained with CD31 (endothelial cells) (red) in the ipsilateral cortex 3 days after TBI. Nuclei were counterstained with DAPI (blue). Scale bar = 20 μm. G Quantification of endothelial expression of ZO-1 in the ipsilateral cortex 3 days after TBI ( n = 6 per group). H Quantification of endothelial expression of TUNEL in the ipsilateral cortex 3 days after TBI ( n = 6 per group). I Representative macroscopic images of Evans Blue extravasation (blue areas) in brain tissue 3 days after TBI. J Quantitative analysis of Evans Blue leakage in ipsilateral hemispheres ( n = 6 per group). Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Journal: Journal of Neuroinflammation

    Article Title: IL-25–ILC2–IL-13 axis improves traumatic brain injury by mediating CXCL-10-dependent regulation of blood brain barrier integrity

    doi: 10.1186/s12974-026-03696-4

    Figure Lengend Snippet: IL-13 improves BBB function by reducing CXCL-10 expression. A - D Western blot analysis of TJs (ZO-1, Occludin, Claudin-5) in the ipsilateral cortex 3 days after TBI: Representative blots ( A ), ZO-1 quantification ( B ), Occludin quantification ( C ), Claudin-5 quantification ( D ) ( n = 6 per group). E Immunofluorescence of ZO-1 (red) co-stained with CD31 (endothelial cells) (green) in the ipsilateral cortex 3 days after TBI. Nuclei were counterstained with DAPI (blue). Scale bar = 50 μm. F Immunofluorescence of TUNEL (green) co-stained with CD31 (endothelial cells) (red) in the ipsilateral cortex 3 days after TBI. Nuclei were counterstained with DAPI (blue). Scale bar = 20 μm. G Quantification of endothelial expression of ZO-1 in the ipsilateral cortex 3 days after TBI ( n = 6 per group). H Quantification of endothelial expression of TUNEL in the ipsilateral cortex 3 days after TBI ( n = 6 per group). I Representative macroscopic images of Evans Blue extravasation (blue areas) in brain tissue 3 days after TBI. J Quantitative analysis of Evans Blue leakage in ipsilateral hemispheres ( n = 6 per group). Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Article Snippet: An anti-mouse IL-13 neutralizing antibody (MAB413, R&D SYSTEMS, USA) was administered via i.p. injection at a dose of 100 μg per mouse 1 day before TBI, followed by daily injections for two consecutive days [ ].

    Techniques: Expressing, Western Blot, Immunofluorescence, Staining, TUNEL Assay

    Graphical abstract: IL-25-activated ILC2s secrete IL-13 to improve BBB function after TBI, by Figdraw

    Journal: Journal of Neuroinflammation

    Article Title: IL-25–ILC2–IL-13 axis improves traumatic brain injury by mediating CXCL-10-dependent regulation of blood brain barrier integrity

    doi: 10.1186/s12974-026-03696-4

    Figure Lengend Snippet: Graphical abstract: IL-25-activated ILC2s secrete IL-13 to improve BBB function after TBI, by Figdraw

    Article Snippet: An anti-mouse IL-13 neutralizing antibody (MAB413, R&D SYSTEMS, USA) was administered via i.p. injection at a dose of 100 μg per mouse 1 day before TBI, followed by daily injections for two consecutive days [ ].

    Techniques: