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mouse il 9 blocking antibody  (Bio X Cell)


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    Bio X Cell mouse il 9 blocking antibody
    Mouse Il 9 Blocking Antibody, supplied by Bio X Cell, used in various techniques. Bioz Stars score: 94/100, based on 22 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+anti+mouse+il+9+blocking+antibody/bio_rxiv__2025__05__05__652112-230-7-11?v=Bio+X+Cell
    Average 94 stars, based on 22 article reviews
    mouse il 9 blocking antibody - by Bioz Stars, 2026-06
    94/100 stars

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    Image Search Results


    Effects of IL-17A mAb treatment on atherosclerotic plaques in Apoe−/− mice. Representative Oil Red O immunohistostainings (original magnification ×4) from aortic root of control [n = 10; (A)]; IL-17A mAb-treated mice [n = 15; (B)] and baseline [n = 5; (C)] are shown. (D–F) Morphometric quantification of cross-sectional area (μm2), fractional stenosis (%), and maximum stenosis (%) of late-stage atherosclerotic lesions were compared. Results are shown as dot plots displaying mean.

    Journal: The Journal of Immunology Author Choice

    Article Title: IL-17A Influences Essential Functions of the Monocyte/Macrophage Lineage and Is Involved in Advanced Murine and Human Atherosclerosis

    doi: 10.4049/jimmunol.1400181

    Figure Lengend Snippet: Effects of IL-17A mAb treatment on atherosclerotic plaques in Apoe−/− mice. Representative Oil Red O immunohistostainings (original magnification ×4) from aortic root of control [n = 10; (A)]; IL-17A mAb-treated mice [n = 15; (B)] and baseline [n = 5; (C)] are shown. (D–F) Morphometric quantification of cross-sectional area (μm2), fractional stenosis (%), and maximum stenosis (%) of late-stage atherosclerotic lesions were compared. Results are shown as dot plots displaying mean.

    Article Snippet: A total of 100 μg blocking mouse IgG1 anti–IL-17A mAb, kindly provided by F. Di Padova (3-784-9; Novartis Institutes for BioMedical Research) ( n = 15), or of isotype IgG1 ( n = 10) was administered i.p. once a week for 16 wk.

    Techniques: Control

    Plaque morphology of the aortic root of Apoe−/− mice. (A) Plaque stability was assessed by quantification of the fibrous cap (μm), collagen content per plaque area (Movat pentachrome staining, original magnification ×4, and two-photon microscopy, original magnification ×40) as well as total number of smooth muscle cells (SMA; original magnification ×40) and apoptotic cells (TUNEL; original magnification ×4) in the lesion. (B) Quantitative analysis of lesion composition of IL-17A mAb–treated (n = 12–15) and control animals (n = 8–10). Results are presented as dot plots displaying mean.

    Journal: The Journal of Immunology Author Choice

    Article Title: IL-17A Influences Essential Functions of the Monocyte/Macrophage Lineage and Is Involved in Advanced Murine and Human Atherosclerosis

    doi: 10.4049/jimmunol.1400181

    Figure Lengend Snippet: Plaque morphology of the aortic root of Apoe−/− mice. (A) Plaque stability was assessed by quantification of the fibrous cap (μm), collagen content per plaque area (Movat pentachrome staining, original magnification ×4, and two-photon microscopy, original magnification ×40) as well as total number of smooth muscle cells (SMA; original magnification ×40) and apoptotic cells (TUNEL; original magnification ×4) in the lesion. (B) Quantitative analysis of lesion composition of IL-17A mAb–treated (n = 12–15) and control animals (n = 8–10). Results are presented as dot plots displaying mean.

    Article Snippet: A total of 100 μg blocking mouse IgG1 anti–IL-17A mAb, kindly provided by F. Di Padova (3-784-9; Novartis Institutes for BioMedical Research) ( n = 15), or of isotype IgG1 ( n = 10) was administered i.p. once a week for 16 wk.

    Techniques: Staining, Microscopy, TUNEL Assay, Control

    Cellular composition in atherosclerotic lesions of Apoe−/− mice. (A) Representative photomicrographs of immunohistochemistry stainings of T cells (CD3, original magnification ×40), Mac-2+ cells (original magnification ×40), CD206+ cells (original magnification ×40), and B cells (B220; original magnification ×40). (B) Quantitative analysis of plaque inflammation are presented in 42-wk-old Apoe−/− mice with (n = 12–15) and without IL-17A mAb treatment (n = 8–10) (as well as 26-wk-old baseline mice, n = 4 to 5). Results are presented as dot plots displaying mean.

    Journal: The Journal of Immunology Author Choice

    Article Title: IL-17A Influences Essential Functions of the Monocyte/Macrophage Lineage and Is Involved in Advanced Murine and Human Atherosclerosis

    doi: 10.4049/jimmunol.1400181

    Figure Lengend Snippet: Cellular composition in atherosclerotic lesions of Apoe−/− mice. (A) Representative photomicrographs of immunohistochemistry stainings of T cells (CD3, original magnification ×40), Mac-2+ cells (original magnification ×40), CD206+ cells (original magnification ×40), and B cells (B220; original magnification ×40). (B) Quantitative analysis of plaque inflammation are presented in 42-wk-old Apoe−/− mice with (n = 12–15) and without IL-17A mAb treatment (n = 8–10) (as well as 26-wk-old baseline mice, n = 4 to 5). Results are presented as dot plots displaying mean.

    Article Snippet: A total of 100 μg blocking mouse IgG1 anti–IL-17A mAb, kindly provided by F. Di Padova (3-784-9; Novartis Institutes for BioMedical Research) ( n = 15), or of isotype IgG1 ( n = 10) was administered i.p. once a week for 16 wk.

    Techniques: Immunohistochemistry

    IL-17A polarizes macrophages toward a distinct proinflammatory transcriptome. (A) Adhesion of monocytes to endothelial cells under static conditions. HUVEC monolayers were pretreated with IL-17A or TNF-α, and monocytes were added for additional 30 min at 37°C in a humidified 5% CO2/95% air mixture. Nonadherent cells were removed by washing twice with PBS. Adherent monocytes were quantitated by direct phase-contrast microscopy. Mean ± SEM of nine independent static adhesion assay experiments. *Versus unstimulated HUVECs, all p < 0.05. (B) Heat map of genes regulated by IL-17A (10 ng/ml for 18 h) as determined by LPE analysis (FDR < 0.05). (C) Expression of selected proinflammatory cytokines, chemokines, surface receptors, and costimulatory molecules significantly regulated by IL-17A (*p < 0.05, †p < 0.01, ‡p < 0.001). (D) GSEA assessing overexpression of predefined gene sets based on transcriptomic analyses of M1 (LPS and IFN-γ), M2 (IL-4), or M4 (CXCL4) macrophages. (E) Hierarchical clustering of IL-17A–treated macrophages and M1 (LPS and IFN-γ), M2 (IL-4), or M4 (CXCL4) macrophages.

    Journal: The Journal of Immunology Author Choice

    Article Title: IL-17A Influences Essential Functions of the Monocyte/Macrophage Lineage and Is Involved in Advanced Murine and Human Atherosclerosis

    doi: 10.4049/jimmunol.1400181

    Figure Lengend Snippet: IL-17A polarizes macrophages toward a distinct proinflammatory transcriptome. (A) Adhesion of monocytes to endothelial cells under static conditions. HUVEC monolayers were pretreated with IL-17A or TNF-α, and monocytes were added for additional 30 min at 37°C in a humidified 5% CO2/95% air mixture. Nonadherent cells were removed by washing twice with PBS. Adherent monocytes were quantitated by direct phase-contrast microscopy. Mean ± SEM of nine independent static adhesion assay experiments. *Versus unstimulated HUVECs, all p < 0.05. (B) Heat map of genes regulated by IL-17A (10 ng/ml for 18 h) as determined by LPE analysis (FDR < 0.05). (C) Expression of selected proinflammatory cytokines, chemokines, surface receptors, and costimulatory molecules significantly regulated by IL-17A (*p < 0.05, †p < 0.01, ‡p < 0.001). (D) GSEA assessing overexpression of predefined gene sets based on transcriptomic analyses of M1 (LPS and IFN-γ), M2 (IL-4), or M4 (CXCL4) macrophages. (E) Hierarchical clustering of IL-17A–treated macrophages and M1 (LPS and IFN-γ), M2 (IL-4), or M4 (CXCL4) macrophages.

    Article Snippet: A total of 100 μg blocking mouse IgG1 anti–IL-17A mAb, kindly provided by F. Di Padova (3-784-9; Novartis Institutes for BioMedical Research) ( n = 15), or of isotype IgG1 ( n = 10) was administered i.p. once a week for 16 wk.

    Techniques: Microscopy, Cell Adhesion Assay, Expressing, Over Expression

    Effects of IL-17A on monocytes and monocyte-derived cells. (A and B) Foam cell formation assay. (A) Representative photomicrographs of monocyte-derived macrophages incubated with oxLDL in addition to IL-17A in different concentrations are shown (original magnification ×20). Representative Oil Red O staining of different groups are shown: no oxLDL (control), oxLDL, and oxLDL plus IL-17A. (B) Data are given as mean ± SEM of five independent experiments. (C) oxLDL uptake assay. Flow cytometry analysis of DiI-labeled oxLDL uptake (in addition to IL-17A incubation) of monocyte-derived macrophages: solid green line (oxLDL) and dotted pink line (oxLDL+IL-17A). Histogram represents one out of three independent experiments. (D) For T cell activation assays, macrophages or DCs were incubated in 96-well round-bottom plates and stimulated with oxLDL (Sanbio), IL-17A (R&D Systems), or oxLDL in combination with IL-17A. After 6-h preincubation, CD4+ T cells were added in a ratio of 1:5 and stimulated for 8 h. Expression of activation-associated cytokines and transcription factors in CD4+ T cells was measured (see Materials and Methods for details). Representative analysis of T-box21 (T-bet), IL2, and IFNγ are shown.

    Journal: The Journal of Immunology Author Choice

    Article Title: IL-17A Influences Essential Functions of the Monocyte/Macrophage Lineage and Is Involved in Advanced Murine and Human Atherosclerosis

    doi: 10.4049/jimmunol.1400181

    Figure Lengend Snippet: Effects of IL-17A on monocytes and monocyte-derived cells. (A and B) Foam cell formation assay. (A) Representative photomicrographs of monocyte-derived macrophages incubated with oxLDL in addition to IL-17A in different concentrations are shown (original magnification ×20). Representative Oil Red O staining of different groups are shown: no oxLDL (control), oxLDL, and oxLDL plus IL-17A. (B) Data are given as mean ± SEM of five independent experiments. (C) oxLDL uptake assay. Flow cytometry analysis of DiI-labeled oxLDL uptake (in addition to IL-17A incubation) of monocyte-derived macrophages: solid green line (oxLDL) and dotted pink line (oxLDL+IL-17A). Histogram represents one out of three independent experiments. (D) For T cell activation assays, macrophages or DCs were incubated in 96-well round-bottom plates and stimulated with oxLDL (Sanbio), IL-17A (R&D Systems), or oxLDL in combination with IL-17A. After 6-h preincubation, CD4+ T cells were added in a ratio of 1:5 and stimulated for 8 h. Expression of activation-associated cytokines and transcription factors in CD4+ T cells was measured (see Materials and Methods for details). Representative analysis of T-box21 (T-bet), IL2, and IFNγ are shown.

    Article Snippet: A total of 100 μg blocking mouse IgG1 anti–IL-17A mAb, kindly provided by F. Di Padova (3-784-9; Novartis Institutes for BioMedical Research) ( n = 15), or of isotype IgG1 ( n = 10) was administered i.p. once a week for 16 wk.

    Techniques: Derivative Assay, Tube Formation Assay, Incubation, Staining, Control, Flow Cytometry, Labeling, Activation Assay, Expressing

    (Synergistic) effects of IL-17A stimulation on the inflammatory milieu in human carotid plaque tissues. Pieces of lipid-rich plaque tissue were stimulated with 10 ng/ml IL-17A, LPS (1 μg/ml), TNF-α (5 ng/ml), IFN-γ (10 ng/ml), or combined and compared with an unstimulated part of the plaque (n = 5–12, respectively). Transcripts of MCP-1 (CCL2) and MMP9 after 8 h, CXCL1 and collagen type 1 after 3 h (A), as well as TNFα and IL6 (B) after 8 h and ICAM1 after 3 h (B) were measured by quantitative RT-PCR and adjusted to β-actin copies. *p = 0.02 versus LPS-stimulated plaques, †p = 0.04 versus IL-17A–stimulated plaque tissue, and ‡p < 0.01versus unstimulated plaque pieces.

    Journal: The Journal of Immunology Author Choice

    Article Title: IL-17A Influences Essential Functions of the Monocyte/Macrophage Lineage and Is Involved in Advanced Murine and Human Atherosclerosis

    doi: 10.4049/jimmunol.1400181

    Figure Lengend Snippet: (Synergistic) effects of IL-17A stimulation on the inflammatory milieu in human carotid plaque tissues. Pieces of lipid-rich plaque tissue were stimulated with 10 ng/ml IL-17A, LPS (1 μg/ml), TNF-α (5 ng/ml), IFN-γ (10 ng/ml), or combined and compared with an unstimulated part of the plaque (n = 5–12, respectively). Transcripts of MCP-1 (CCL2) and MMP9 after 8 h, CXCL1 and collagen type 1 after 3 h (A), as well as TNFα and IL6 (B) after 8 h and ICAM1 after 3 h (B) were measured by quantitative RT-PCR and adjusted to β-actin copies. *p = 0.02 versus LPS-stimulated plaques, †p = 0.04 versus IL-17A–stimulated plaque tissue, and ‡p < 0.01versus unstimulated plaque pieces.

    Article Snippet: A total of 100 μg blocking mouse IgG1 anti–IL-17A mAb, kindly provided by F. Di Padova (3-784-9; Novartis Institutes for BioMedical Research) ( n = 15), or of isotype IgG1 ( n = 10) was administered i.p. once a week for 16 wk.

    Techniques: Quantitative RT-PCR

    Quantitative supernatant ELISA results for different cytokines and chemokines from plaque culture experiments

    Journal: The Journal of Immunology Author Choice

    Article Title: IL-17A Influences Essential Functions of the Monocyte/Macrophage Lineage and Is Involved in Advanced Murine and Human Atherosclerosis

    doi: 10.4049/jimmunol.1400181

    Figure Lengend Snippet: Quantitative supernatant ELISA results for different cytokines and chemokines from plaque culture experiments

    Article Snippet: A total of 100 μg blocking mouse IgG1 anti–IL-17A mAb, kindly provided by F. Di Padova (3-784-9; Novartis Institutes for BioMedical Research) ( n = 15), or of isotype IgG1 ( n = 10) was administered i.p. once a week for 16 wk.

    Techniques: Enzyme-linked Immunosorbent Assay