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biotinylated goat anti human ccl5 rantes antibody  (R&D Systems)


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    R&D Systems biotinylated goat anti human ccl5 rantes antibody
    Biotinylated Goat Anti Human Ccl5 Rantes Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 13 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/biotinylated goat anti human ccl5 rantes antibody/product/R&D Systems
    Average 93 stars, based on 13 article reviews
    biotinylated goat anti human ccl5 rantes antibody - by Bioz Stars, 2026-03
    93/100 stars

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    R&D Systems biotinylated anti mouse ccl5
    Figure 1. The Effect of IFNb on Cultured Bone Marrow-Derived Macrophages (A) Treatment of macrophages with IFNb induces IL-10 expression without affecting TNF or IL-12. (B) Uptake of DiI-labeled oxLDL by control (ctrl)- or IFNb-treated macrophages. (C) Uptake of fluorescent latex beads by ctrl- or IFNb-treated macrophages. (D) Surface expression of VLA-4, Mac1, LFA-1, and PSGL1 in ctrl- or IFNb-treated macrophages. (E) Relative gene expression of chemokine receptors in ctrl- or IFNb-treated macrophages. (F) Chemokine expression after IFNb treatment of macrophages. (G) FACS analysis of CCR2 and CCR5 after treatment with IFNb. (H) <t>CCL5</t> secretion by macrophages after treatment with IFNb. (I) CCL5 expression in ctrl- and IFNb-stimulated IFNAR1WT and IFNAR1del macrophages. (J) CCL5 expression in ctrl- or IFNb-treated wild-type and STAT1/ macrophages. Graphs are representative for at least two independent experiments. Bars represent mean of triplicate wells ± SEM. *p < 0.05, **p < 0.01.
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    R&D Systems baf478
    Figure 1. The Effect of IFNb on Cultured Bone Marrow-Derived Macrophages (A) Treatment of macrophages with IFNb induces IL-10 expression without affecting TNF or IL-12. (B) Uptake of DiI-labeled oxLDL by control (ctrl)- or IFNb-treated macrophages. (C) Uptake of fluorescent latex beads by ctrl- or IFNb-treated macrophages. (D) Surface expression of VLA-4, Mac1, LFA-1, and PSGL1 in ctrl- or IFNb-treated macrophages. (E) Relative gene expression of chemokine receptors in ctrl- or IFNb-treated macrophages. (F) Chemokine expression after IFNb treatment of macrophages. (G) FACS analysis of CCR2 and CCR5 after treatment with IFNb. (H) <t>CCL5</t> secretion by macrophages after treatment with IFNb. (I) CCL5 expression in ctrl- and IFNb-stimulated IFNAR1WT and IFNAR1del macrophages. (J) CCL5 expression in ctrl- or IFNb-treated wild-type and STAT1/ macrophages. Graphs are representative for at least two independent experiments. Bars represent mean of triplicate wells ± SEM. *p < 0.05, **p < 0.01.
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    Figure 1. The Effect of IFNb on Cultured Bone Marrow-Derived Macrophages (A) Treatment of macrophages with IFNb induces IL-10 expression without affecting TNF or IL-12. (B) Uptake of DiI-labeled oxLDL by control (ctrl)- or IFNb-treated macrophages. (C) Uptake of fluorescent latex beads by ctrl- or IFNb-treated macrophages. (D) Surface expression of VLA-4, Mac1, LFA-1, and PSGL1 in ctrl- or IFNb-treated macrophages. (E) Relative gene expression of chemokine receptors in ctrl- or IFNb-treated macrophages. (F) Chemokine expression after IFNb treatment of macrophages. (G) FACS analysis of CCR2 and CCR5 after treatment with IFNb. (H) CCL5 secretion by macrophages after treatment with IFNb. (I) CCL5 expression in ctrl- and IFNb-stimulated IFNAR1WT and IFNAR1del macrophages. (J) CCL5 expression in ctrl- or IFNb-treated wild-type and STAT1/ macrophages. Graphs are representative for at least two independent experiments. Bars represent mean of triplicate wells ± SEM. *p < 0.05, **p < 0.01.

    Journal: Cell metabolism

    Article Title: Myeloid type I interferon signaling promotes atherosclerosis by stimulating macrophage recruitment to lesions.

    doi: 10.1016/j.cmet.2010.06.008

    Figure Lengend Snippet: Figure 1. The Effect of IFNb on Cultured Bone Marrow-Derived Macrophages (A) Treatment of macrophages with IFNb induces IL-10 expression without affecting TNF or IL-12. (B) Uptake of DiI-labeled oxLDL by control (ctrl)- or IFNb-treated macrophages. (C) Uptake of fluorescent latex beads by ctrl- or IFNb-treated macrophages. (D) Surface expression of VLA-4, Mac1, LFA-1, and PSGL1 in ctrl- or IFNb-treated macrophages. (E) Relative gene expression of chemokine receptors in ctrl- or IFNb-treated macrophages. (F) Chemokine expression after IFNb treatment of macrophages. (G) FACS analysis of CCR2 and CCR5 after treatment with IFNb. (H) CCL5 secretion by macrophages after treatment with IFNb. (I) CCL5 expression in ctrl- and IFNb-stimulated IFNAR1WT and IFNAR1del macrophages. (J) CCL5 expression in ctrl- or IFNb-treated wild-type and STAT1/ macrophages. Graphs are representative for at least two independent experiments. Bars represent mean of triplicate wells ± SEM. *p < 0.05, **p < 0.01.

    Article Snippet: Murine CCL5 secretion from BMM (± 100 U/ml IFNb for 24 hr) was measured by ELISA using anti-mouse CCL5 (R&D Systems, Abigndon, UK) as coating antibody and biotinylated anti-mouse CCL5 (R&D Systems) as detection antibody with mouse CCL5 (Peprotech) as standard.

    Techniques: Cell Culture, Derivative Assay, Expressing, Labeling, Control, Gene Expression

    Figure 3. IFNb Treatment Accelerates Atherosclerosis in apoe/ and ldlr/ Mice (A) Representative lesions of ctrl- or IFNb treated mice of collar-induced atherosclerosis in apoe/ mice. Scale bar, 50 mm. (B) Lesion area measured at six sequential locations proximal from the collar in apoe/ mice that were ctrl or IFNb treated. **p < 0.01 by two-way ANOVA; n = 9/12. (C) Representative lesions in the aortic root of ctrl- or IFNb-treated ldlr/ mice. Scale bar, 200 mm. (D) Lesion area at the aortic root of ctrl- or IFNb-treated ldlr/ mice. *p < 0.05; n = 12/14. (E) Representative MOMA-2-stained lesions from ctrl- and IFNb-treated ldlr/ mice. Scale bar, 100 mm. (F) Absolute macrophage area in lesions from ctrl- or IFNb-treated ldlr/ mice. *p < 0.05; n = 12/14. (G) CD68 expression in aortic arches from ctrl- or IFNb-treated ldlr/ mice. **p < 0.01; n = 11/14. (H) CCL5 levels in plasma from ctrl- or IFNb-treated ldlr/ mice. **p < 0.01; n = 9/11. Shown are mean ± SEM.

    Journal: Cell metabolism

    Article Title: Myeloid type I interferon signaling promotes atherosclerosis by stimulating macrophage recruitment to lesions.

    doi: 10.1016/j.cmet.2010.06.008

    Figure Lengend Snippet: Figure 3. IFNb Treatment Accelerates Atherosclerosis in apoe/ and ldlr/ Mice (A) Representative lesions of ctrl- or IFNb treated mice of collar-induced atherosclerosis in apoe/ mice. Scale bar, 50 mm. (B) Lesion area measured at six sequential locations proximal from the collar in apoe/ mice that were ctrl or IFNb treated. **p < 0.01 by two-way ANOVA; n = 9/12. (C) Representative lesions in the aortic root of ctrl- or IFNb-treated ldlr/ mice. Scale bar, 200 mm. (D) Lesion area at the aortic root of ctrl- or IFNb-treated ldlr/ mice. *p < 0.05; n = 12/14. (E) Representative MOMA-2-stained lesions from ctrl- and IFNb-treated ldlr/ mice. Scale bar, 100 mm. (F) Absolute macrophage area in lesions from ctrl- or IFNb-treated ldlr/ mice. *p < 0.05; n = 12/14. (G) CD68 expression in aortic arches from ctrl- or IFNb-treated ldlr/ mice. **p < 0.01; n = 11/14. (H) CCL5 levels in plasma from ctrl- or IFNb-treated ldlr/ mice. **p < 0.01; n = 9/11. Shown are mean ± SEM.

    Article Snippet: Murine CCL5 secretion from BMM (± 100 U/ml IFNb for 24 hr) was measured by ELISA using anti-mouse CCL5 (R&D Systems, Abigndon, UK) as coating antibody and biotinylated anti-mouse CCL5 (R&D Systems) as detection antibody with mouse CCL5 (Peprotech) as standard.

    Techniques: Staining, Expressing, Clinical Proteomics

    Figure 6. IFNb Induces Chemotactic Factors in Human Primary Macrophages, and Type I IFN Signaling Is Upregulated in Ruptured Human Atherosclerotic Lesions (A) CCR2 expression in macrophages from two independent donors after IFNb treatment. (B) CCR5 expression in macrophages from two independent donors after IFNb treatment. *p < 0.05; **p < 0.01. (C) CCL5 expression in macrophages from two independent donors after IFNb treatment. **p < 0.01. Error bars indicate mean of triplicate wells ± SEM. (D) Ingenuity Pathway Analysis of the differentially expressed genes in stable compared to ruptured carotid endarterectomy specimens. Red signals indicate upregulation and the pathway showed a strongly significant (p = 2.36 3 106; ratio 16/23 [0.696]) upregulation of type I IFN signaling. Indicated are the fold changes (FC) of the respective genes.

    Journal: Cell metabolism

    Article Title: Myeloid type I interferon signaling promotes atherosclerosis by stimulating macrophage recruitment to lesions.

    doi: 10.1016/j.cmet.2010.06.008

    Figure Lengend Snippet: Figure 6. IFNb Induces Chemotactic Factors in Human Primary Macrophages, and Type I IFN Signaling Is Upregulated in Ruptured Human Atherosclerotic Lesions (A) CCR2 expression in macrophages from two independent donors after IFNb treatment. (B) CCR5 expression in macrophages from two independent donors after IFNb treatment. *p < 0.05; **p < 0.01. (C) CCL5 expression in macrophages from two independent donors after IFNb treatment. **p < 0.01. Error bars indicate mean of triplicate wells ± SEM. (D) Ingenuity Pathway Analysis of the differentially expressed genes in stable compared to ruptured carotid endarterectomy specimens. Red signals indicate upregulation and the pathway showed a strongly significant (p = 2.36 3 106; ratio 16/23 [0.696]) upregulation of type I IFN signaling. Indicated are the fold changes (FC) of the respective genes.

    Article Snippet: Murine CCL5 secretion from BMM (± 100 U/ml IFNb for 24 hr) was measured by ELISA using anti-mouse CCL5 (R&D Systems, Abigndon, UK) as coating antibody and biotinylated anti-mouse CCL5 (R&D Systems) as detection antibody with mouse CCL5 (Peprotech) as standard.

    Techniques: Expressing