anti mil 17b function blocking antibody  (R&D Systems)

Journal: Cell reports

Article Title: IL-17/CXCL5 signaling within the oligovascular niche mediates human and mouse white matter injury

doi: 10.1016/j.celrep.2022.111848

Figure Lengend Snippet: Human brain microvascular endothelial cells were stimulated with IL-17 ligands A–E (250 ng/mL) and CXCL5 levels measured in conditioned media 48 h after stimulation (*p = 0.0372 by Kruskal-Wallis H test; **post-hoc comparison for IL-17B versus no ligand, adjusted p = 0.0178) (A). Phalloidin+ cellular area in O4+ OPCs grown in vitro exposed to vehicle (top panel) or recombinant CXCL5 (bottom panel) for 48 h (p < 0.0001, F = 9.82 by one-way ANOVA) (B). Approach for CXCL5 transgenic-viral gain of function in subcortical white matter of Tie2-Cre;tdTomato mice (top panel) (C). PDGFRα+ OPC (green) labeling in GFP-transduced Tie2-Cre;tdTomato mice (red, left panel) and CXCL5-GFP-transduced Tie2-Cre;tdTomato mice (right panel). Representative masked cellular profiles of PDGFRα+ cell area (bottom panels). Schematic of anti-IL-17B antibody treatment (top panel) (D). PDGFRα+ OPC (green) labeling in control IgG-treated Tie2-Cre:tdT mice (left panel) and anti-IL-17B IgG-treated Tie2-Cre:tdT mice (right panel). Representative masked cellular profiles of PDGFRα+ cell area (bottom panels). Proportion of OPCs per unit distance from vessel (0–35 μm) in each condition (total measured cell number per condition in parentheses) (E). Average distance of OPCs to vessel (***p = 0.0005, F = 6.06 by one-way ANOVA; **adjusted p = 0.0039; *adjusted p = 0.0168) (F). Average in vivo PDGFRα+ OPC cell area (**p = 0.0068, F = 7.38 by one-way ANOVA; **adjusted p = 0.002) (G). Graph of co-localized CXCL5+/GLUT-1+ voxels in anti-IL-17B IgG-treated animals (n = 4/grp; *p = 0.018) (H). Error bars represent S.E.M. Scale bars: 10 μm

Article Snippet: Anti-mIL-17B function blocking antibody (R&D, AF1709) was diluted with 0.9% saline to a concentration of 1 mg/mL.

Techniques: Comparison, In Vitro, Recombinant, Transgenic Assay, Labeling, Control, In Vivo

Journal: Cell reports

Article Title: IL-17/CXCL5 signaling within the oligovascular niche mediates human and mouse white matter injury

doi: 10.1016/j.celrep.2022.111848

Figure Lengend Snippet: Plasma levels of log 10 -CXCL5 in ASPIRE cohort subjects separated by detectable plasma IL-17B (n = 32; median 1043.0 pg/mL) compared with those with undetectable plasma IL-17B (n = 99; median 515.3 pg/mL; *p < 0.0001). Plasma log 10 -CXCL5 levels in subjects with MRI-confirmed acute microvascular ischemia (IL-17B + subjects; n = 9; 978.2 pg/mL versus IL-17B− subjects; n = 24; 539.7 pg/mL) (**p = 0.0157) (A). Ordinal shift analysis of modified Fazekas scale scores from plasma IL-17B+ and IL-17B− subjects (p < 0.0001) (B). Representative immunohistochemical detection of CXCL5 in human frontal white matter vasculature in subjects with cerebrovascular pathology (C). Percentage of CXCL5+ vessel segments in peri-ventricular white matter (n = 10) (p = 0.0005). Error bars represent S.E.M. Scale bar: 10 μm

Article Snippet: Anti-mIL-17B function blocking antibody (R&D, AF1709) was diluted with 0.9% saline to a concentration of 1 mg/mL.

Techniques: Clinical Proteomics, Modification, Immunohistochemical staining

Journal: Cell reports

Article Title: IL-17/CXCL5 signaling within the oligovascular niche mediates human and mouse white matter injury

doi: 10.1016/j.celrep.2022.111848

Figure Lengend Snippet:

Article Snippet: Anti-mIL-17B function blocking antibody (R&D, AF1709) was diluted with 0.9% saline to a concentration of 1 mg/mL.

Techniques: Blocking Assay, Virus, Recombinant, Enzyme-linked Immunosorbent Assay, Luminex, Hybridization, Plasmid Preparation, Biomarker Discovery, Control, Software

Journal: bioRxiv

Article Title: Endothelial CXCL5 negatively regulates myelination and repair after white matter stroke

doi: 10.1101/664953

Figure Lengend Snippet: Schematic representation of IL-17/CXCL5 signaling in chronically injured cerebral endothelia (A). Human brain microvascular endothelial cells were stimulated with IL-17 ligands A-E (250 ng/mL) and CXCL5 levels measured in conditioned media 48 hrs after stimulation (* p =0.0372 by Kruskal-Wallis H test; **post-hoc comparison for IL-17B vs. no ligand, adjusted p =0.0178) (B). Weight adjusted-ELISA values (pg/mL) for murine CXCL5 in retro-orbital blood samples from CFD (black) and HFD (red) animals ( n =4/grp, p =0.0355) (C). Immunofluorescence labeling for IL-17Rb (green, D) and CXCL5 (green, E) is absent in white matter vasculature of Tie2-Cre;tdTomato mice on CFD (left panels) and abundant in white matter vasculature of Tie2-Cre;tdTomato mice on HFD (right panels). Single channel labeling for IL17Rb (lower panels, D) and CXCL5 (lower panels, E) show heterogenous endothelial expression. CXCL5 is detected in human frontal white matter endothelia from aged subjects. Bar represents percentage of cases (8/10) with any CXCL5 staining with points indicating the individual percentage of CXCL5-positive vessel segments in individuals with (blue) and without (red) vascular dementia (F). Scale bars = 50 μm in F, 20 μm in D, 10 μm in E.

Article Snippet: Anti-mIL-17B function blocking antibody (R&D, AF1709) was diluted with 0.9% saline to a concentration of 1mg/ml.

Techniques: Enzyme-linked Immunosorbent Assay, Immunofluorescence, Labeling, Expressing, Staining

Journal: bioRxiv

Article Title: Endothelial CXCL5 negatively regulates myelination and repair after white matter stroke

doi: 10.1101/664953

Figure Lengend Snippet: Association of PDGFRα+ OPCs (green) with the vasculature (blue) in CFD (upper panel) and CXCL5-positive (red) HFD animals (lower panel) (A). Phalloidin-positive cellular area in O4+ OPCs grown in vitro exposed to vehicle (upper panel) or recombinant CXCL5 (lower panel) for 48 h ( p <0.0001, F=9.82 by one-way ANOVA). Experimental approach for CXCL5 transgenic-viral gain of function (upper panel, C). PDGFRα+ OPC (green) labeling in GFP-transduced Tie2-Cre;tdTomato mice (red, left panel) and CXCL5-GFP-transduced Tie2-Cre;tdTomato mice (right panel). Representative masked cellular profiles of PDGFRα+ cell area (lower panels). Schematic of anti-IL-17B antibody treatment (upper panel, D). PDGFRα+ OPC (green) labeling in control IgG-treated Tie2-Cre:tdT mice (left panel) and anti-IL-17B IgG-treated Tie2-Cre:tdT mice (right panel). Representative masked cellular profiles of PDGFRα+ cell area (lower panels). Proportion of OPCs per unit distance from vessel (0-35 μm) in each condition (total measured cell number per condition in parentheses) (E). Average distance of OPCs to vessel (*** p =0.0005, F=6.06 by one-way ANOVA; **adjusted p =0.0039; *adjusted p =0.0168) (F). Average in vivo PDGFRα+ OPC cell area (** p =0.0068, F=7.38 by one-way ANOVA; **adjusted p =0.002) (G). Graph of co-localized CXCL5+/GLUT-1+ voxels in anti-IL-17B IgG-treated animals ( n= 4/grp; *p =0.018). (H). Scale bars = 10 μm.

Article Snippet: Anti-mIL-17B function blocking antibody (R&D, AF1709) was diluted with 0.9% saline to a concentration of 1mg/ml.

Techniques: In Vitro, Recombinant, Transgenic Assay, Labeling, In Vivo

Journal: bioRxiv

Article Title: Endothelial CXCL5 negatively regulates myelination and repair after white matter stroke

doi: 10.1101/664953

Figure Lengend Snippet: Subjects presenting for evaluation of acute neurologic deficits were enrolled in the ASPIRE study cohort (A). In all subjects, serum levels of CXCL5 were elevated in those subjects with detectable serum IL-17B ( n =32; median 1043.0 pg/mL) compared to those with undetectable serum IL-17B ( n =99; median 515.3 pg/mL; * p <0.0001; Mann-Whitney). Among those subjects with MRI-confirmed acute microvascular ischemia, serum CXCL5 levels were higher in IL-17B+ subjects ( n =9; 978.2 pg/mL) vs. IL-17B-subjects ( n =24; 539.7 pg/mL) (** p =0.0157; Mann Whitney) (B). Box and violin plot of modified Fazekas score in IL-17B+ vs. IL-17B-subjects (dashed line = median) ( p =0.42; Mann-Whitney U-test) (C).

Article Snippet: Anti-mIL-17B function blocking antibody (R&D, AF1709) was diluted with 0.9% saline to a concentration of 1mg/ml.

Techniques: MANN-WHITNEY, Modification