anti cd11b primary antibody Search Results


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  • 93
    Miltenyi Biotec anti cd11b antibody
    Myeloid cells of LysM-Cre/Ikkβ F/F mice are relatively refractory to M1-like proinflammatory activation. a <t>CD11b</t> + cells were isolated from the lumbar spinal cord of adult WT and LysM-Cre/Ikkβ F/F mice using CD11b microbeads. Genomic DNA from CD11b + cells of each group was analyzed by real-time RT-PCR to determine the rate of ikkβ deletion. b Macrophages obtained from normal WT and LysM-Cre/Ikkβ F/F mice were stimulated for 6 h with lipopolysaccharide. Macrophages were isolated and analyzed to evaluate the degree of activation of TNF-α, IL-1β, IL-6, iNOS, IL-10, and TGF-β with real-time RT-PCR. The levels of gene expressions were compared to normal control. c - e Macrophages derived from WT and LysM-Cre/Ikkβ F/F mice were treated with lipopolysaccharide or IL-4, incubated with PE anti-mouse CD80 ( c ), APC anti-mouse CD86 ( c ), and APC anti-mouse CD206 ( d ), and used for flow cytometry analysis ( c and d ). Alteration in protein expression of M1 (iNOS) and M2 marker (Arginine-1) was analyzed by Western blot analysis ( e ). f - i Semi-thin sections from the lumbar spinal cord of adult WT (F and H) and LysM-Cre/Ikkβ F/F mice ( g and i ) were stained with toluidine blue. Panels h and i display high magnification micrographs of sections in (panels f and g ) marked with squares, respectively. Bars = 100 μm. j - m Spinal cord lysate obtained from adult WT and LysM-Cre/Ikkβ F/F mice was analyzed for the expression of MBP by immunoblotting ( j ) and were quantified ( k ). The same preparation was analyzed for mRNA expression of MBP by real-time RT-PCR ( l ) and was quantified ( m ). Data are representative of 3 independent experiments with similar results. (ANOVA test; ** p
    Anti Cd11b Antibody, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti cd11b antibody/product/Miltenyi Biotec
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti cd11b antibody - by Bioz Stars, 2021-06
    93/100 stars
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    cd11b  (Abcam)
    99
    Abcam cd11b
    Factor XIIIA in IMs promotes fibrin cross-linking and LUSC invasion. a Relative mRNA expression of F13a1 from sorted IMs and RMs, n = 3 mice. b Immunofluorescent (IF) imaging of IMs and RMs comparing FXIIIA (red) expression. c Dual staining for FXIIIA (red) and <t>CD11b</t> (green) in IMs. Contents of dotted white box are enlarged under each panel. d Confocal imaging of IMs for FXIIIA (red). White arrows point toward podosome-like structures. Scale bar: 5 μm; nuclei were stained with Hoechst (panels b – d ). e Fibrin cross-linking patterns by western blotting using a polyclonal anti-human fibrin(ogen) antibody using freshly sorted IMs and RMs (Low = 25k cells, High = 100k cells), with or without the FXIIIA-inhibitor, T101. f Percent invadopodia of LN4K1 cells growing in either unfractionated (UF Fgn, left) or Peak 1 (FXIIIA-depleted) fibrinogen (right). White arrows show evidence of invadopodia. Scale bar 50 μm. Data are averages ± s.e.m. P -values obtained with Student’s t-test. g Schematic of co-culture model (top). Representative images of LN4K1-GFP cells growing in either UF Fgn or Peak 1 with or without low (100k) or high (300k) IMs. FDR = 0.0001 for all statistical comparisons shown. Groups in e + g treated with the T101 were dosed at 50 μM. Scale bar 12.5 μm. Data are averages ± s.e.m. P -values were obtained with Student’s t-test. h Invaded LN4K1-GFP cells per high power field (HPF) at 24 h following seeding into either UF Fgn or Peak 1 Fgn alone or co-cultured with IMs with or without T101 (50 μM). FDR
    Cd11b, supplied by Abcam, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cd11b/product/Abcam
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    cd11b - by Bioz Stars, 2021-06
    99/100 stars
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    86
    Abcam anti cd11b antibody epr1344
    Presenting melatonin at histochemical and RNA levels inhibits chronic inflammation in the lungs of mice exposed to LPS. (A–C) Significantly fewer CD45+ T cells, <t>CD11b+</t> and CD11c+ and F4/80+ macrophages infiltrated into mouse lung bronchi and alveoli when LPS-exposed mice were given melatonin orally daily than non-treated mice. Luzindole (MT1/MT2 inhibitor) increased the infiltration of these inflammatory cells into the mouse lung, even when the mice were treated with melatonin. N = 5–7. (D) Mice treated with melatonin expressed lower levels of Il-6, Il-1β, Ifn-γ, and Tnf-α mRNAs as well as more Gpx, Ho-1, Sod1, and Sod2 mRNAs in the lungs than compared with LPS-exposed mice. Mice treated with luzindole (MT1/MT2 inhibitor) along with melatonin had higher levels of Il-6, Ifn-γ, and Tnf-α and decreased Gpx, Ho-1, and Sod1 mRNA expression in the lungs. N = 4–5. *p
    Anti Cd11b Antibody Epr1344, supplied by Abcam, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti cd11b antibody epr1344/product/Abcam
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti cd11b antibody epr1344 - by Bioz Stars, 2021-06
    86/100 stars
      Buy from Supplier

    Image Search Results


    Myeloid cells of LysM-Cre/Ikkβ F/F mice are relatively refractory to M1-like proinflammatory activation. a CD11b + cells were isolated from the lumbar spinal cord of adult WT and LysM-Cre/Ikkβ F/F mice using CD11b microbeads. Genomic DNA from CD11b + cells of each group was analyzed by real-time RT-PCR to determine the rate of ikkβ deletion. b Macrophages obtained from normal WT and LysM-Cre/Ikkβ F/F mice were stimulated for 6 h with lipopolysaccharide. Macrophages were isolated and analyzed to evaluate the degree of activation of TNF-α, IL-1β, IL-6, iNOS, IL-10, and TGF-β with real-time RT-PCR. The levels of gene expressions were compared to normal control. c - e Macrophages derived from WT and LysM-Cre/Ikkβ F/F mice were treated with lipopolysaccharide or IL-4, incubated with PE anti-mouse CD80 ( c ), APC anti-mouse CD86 ( c ), and APC anti-mouse CD206 ( d ), and used for flow cytometry analysis ( c and d ). Alteration in protein expression of M1 (iNOS) and M2 marker (Arginine-1) was analyzed by Western blot analysis ( e ). f - i Semi-thin sections from the lumbar spinal cord of adult WT (F and H) and LysM-Cre/Ikkβ F/F mice ( g and i ) were stained with toluidine blue. Panels h and i display high magnification micrographs of sections in (panels f and g ) marked with squares, respectively. Bars = 100 μm. j - m Spinal cord lysate obtained from adult WT and LysM-Cre/Ikkβ F/F mice was analyzed for the expression of MBP by immunoblotting ( j ) and were quantified ( k ). The same preparation was analyzed for mRNA expression of MBP by real-time RT-PCR ( l ) and was quantified ( m ). Data are representative of 3 independent experiments with similar results. (ANOVA test; ** p

    Journal: Molecular Neurodegeneration

    Article Title: IKKβ-mediated inflammatory myeloid cell activation exacerbates experimental autoimmune encephalomyelitis by potentiating Th1/Th17 cell activation and compromising blood brain barrier

    doi: 10.1186/s13024-016-0116-1

    Figure Lengend Snippet: Myeloid cells of LysM-Cre/Ikkβ F/F mice are relatively refractory to M1-like proinflammatory activation. a CD11b + cells were isolated from the lumbar spinal cord of adult WT and LysM-Cre/Ikkβ F/F mice using CD11b microbeads. Genomic DNA from CD11b + cells of each group was analyzed by real-time RT-PCR to determine the rate of ikkβ deletion. b Macrophages obtained from normal WT and LysM-Cre/Ikkβ F/F mice were stimulated for 6 h with lipopolysaccharide. Macrophages were isolated and analyzed to evaluate the degree of activation of TNF-α, IL-1β, IL-6, iNOS, IL-10, and TGF-β with real-time RT-PCR. The levels of gene expressions were compared to normal control. c - e Macrophages derived from WT and LysM-Cre/Ikkβ F/F mice were treated with lipopolysaccharide or IL-4, incubated with PE anti-mouse CD80 ( c ), APC anti-mouse CD86 ( c ), and APC anti-mouse CD206 ( d ), and used for flow cytometry analysis ( c and d ). Alteration in protein expression of M1 (iNOS) and M2 marker (Arginine-1) was analyzed by Western blot analysis ( e ). f - i Semi-thin sections from the lumbar spinal cord of adult WT (F and H) and LysM-Cre/Ikkβ F/F mice ( g and i ) were stained with toluidine blue. Panels h and i display high magnification micrographs of sections in (panels f and g ) marked with squares, respectively. Bars = 100 μm. j - m Spinal cord lysate obtained from adult WT and LysM-Cre/Ikkβ F/F mice was analyzed for the expression of MBP by immunoblotting ( j ) and were quantified ( k ). The same preparation was analyzed for mRNA expression of MBP by real-time RT-PCR ( l ) and was quantified ( m ). Data are representative of 3 independent experiments with similar results. (ANOVA test; ** p

    Article Snippet: Single cells were stained with anti-CD11b antibody (Miltenyi Biotec) for 30 min at 4 °C.

    Techniques: Mouse Assay, Activation Assay, Isolation, Quantitative RT-PCR, Derivative Assay, Incubation, Flow Cytometry, Cytometry, Expressing, Marker, Western Blot, Staining

    Myeloid-specific ikkβ gene deletion inhibits the recruitment/infiltration of residential microglia and of peripheral macrophages in spinal cord lesion during EAE. a - n Spinal cord sections were obtained from WT and LysM-Cre/Ikkβ F/F mice ( n = 5) at 15–18 days after immunization, stained with H E dye ( a - d ), and immunostained with anti-Iba-1 ( e - h ) and anti-CD68 antibodies ( i - l ) to investigate the degree of cellular recruitment/infiltration. Representative photographs show ventrolateral white matter of the lumbar spinal cord ( a - l ). The degree of recruitment/infiltration was quantified and the data are expressed as mean score ± SEM ( m and n ). Bars = 100 μm. o Spinal cords from each group ( n = 5) at 15–18 days after immunization were analyzed with real-time RT-PCR. Data are expressed as mean fold induction ± SEM. p and q Spinal cords were dissected from each group ( n = 5) at 15–18 days after immunization to investigate the degree of recruitment/infiltration of macrophages with flow cytometry. Tissues were dissociated, and cells were incubated with APC-conjugated anti-CD11b and PE-conjugated anti-CD45 antibodies. CD11b + cells were divided into CD11b + /CD45 +(high) cells (R2; macrophage) and CD11b + /CD45 +(low) cells (R3; microglia) populations based on CD45 expression levels ( p ), and the percentages of each population are denoted in the graph ( q ). Mean ± SEM values from 3 independent experiments are shown in the graph. r - t Total RNA was isolated from the lumbar spinal cord of each group ( n = 3) at day 15–18 post-immunization to measure the level of the mRNA expression of IL-1β ( r ), TNF-α ( s ), and iNOS ( t ) with real-time RT-PCR. The mRNA level of each gene is presented as the fold induction ± SEM compared with the levels measured in the normal control mice. (ANOVA test; * p

    Journal: Molecular Neurodegeneration

    Article Title: IKKβ-mediated inflammatory myeloid cell activation exacerbates experimental autoimmune encephalomyelitis by potentiating Th1/Th17 cell activation and compromising blood brain barrier

    doi: 10.1186/s13024-016-0116-1

    Figure Lengend Snippet: Myeloid-specific ikkβ gene deletion inhibits the recruitment/infiltration of residential microglia and of peripheral macrophages in spinal cord lesion during EAE. a - n Spinal cord sections were obtained from WT and LysM-Cre/Ikkβ F/F mice ( n = 5) at 15–18 days after immunization, stained with H E dye ( a - d ), and immunostained with anti-Iba-1 ( e - h ) and anti-CD68 antibodies ( i - l ) to investigate the degree of cellular recruitment/infiltration. Representative photographs show ventrolateral white matter of the lumbar spinal cord ( a - l ). The degree of recruitment/infiltration was quantified and the data are expressed as mean score ± SEM ( m and n ). Bars = 100 μm. o Spinal cords from each group ( n = 5) at 15–18 days after immunization were analyzed with real-time RT-PCR. Data are expressed as mean fold induction ± SEM. p and q Spinal cords were dissected from each group ( n = 5) at 15–18 days after immunization to investigate the degree of recruitment/infiltration of macrophages with flow cytometry. Tissues were dissociated, and cells were incubated with APC-conjugated anti-CD11b and PE-conjugated anti-CD45 antibodies. CD11b + cells were divided into CD11b + /CD45 +(high) cells (R2; macrophage) and CD11b + /CD45 +(low) cells (R3; microglia) populations based on CD45 expression levels ( p ), and the percentages of each population are denoted in the graph ( q ). Mean ± SEM values from 3 independent experiments are shown in the graph. r - t Total RNA was isolated from the lumbar spinal cord of each group ( n = 3) at day 15–18 post-immunization to measure the level of the mRNA expression of IL-1β ( r ), TNF-α ( s ), and iNOS ( t ) with real-time RT-PCR. The mRNA level of each gene is presented as the fold induction ± SEM compared with the levels measured in the normal control mice. (ANOVA test; * p

    Article Snippet: Single cells were stained with anti-CD11b antibody (Miltenyi Biotec) for 30 min at 4 °C.

    Techniques: Mouse Assay, Staining, Quantitative RT-PCR, Flow Cytometry, Cytometry, Incubation, Expressing, Isolation

    Factor XIIIA in IMs promotes fibrin cross-linking and LUSC invasion. a Relative mRNA expression of F13a1 from sorted IMs and RMs, n = 3 mice. b Immunofluorescent (IF) imaging of IMs and RMs comparing FXIIIA (red) expression. c Dual staining for FXIIIA (red) and CD11b (green) in IMs. Contents of dotted white box are enlarged under each panel. d Confocal imaging of IMs for FXIIIA (red). White arrows point toward podosome-like structures. Scale bar: 5 μm; nuclei were stained with Hoechst (panels b – d ). e Fibrin cross-linking patterns by western blotting using a polyclonal anti-human fibrin(ogen) antibody using freshly sorted IMs and RMs (Low = 25k cells, High = 100k cells), with or without the FXIIIA-inhibitor, T101. f Percent invadopodia of LN4K1 cells growing in either unfractionated (UF Fgn, left) or Peak 1 (FXIIIA-depleted) fibrinogen (right). White arrows show evidence of invadopodia. Scale bar 50 μm. Data are averages ± s.e.m. P -values obtained with Student’s t-test. g Schematic of co-culture model (top). Representative images of LN4K1-GFP cells growing in either UF Fgn or Peak 1 with or without low (100k) or high (300k) IMs. FDR = 0.0001 for all statistical comparisons shown. Groups in e + g treated with the T101 were dosed at 50 μM. Scale bar 12.5 μm. Data are averages ± s.e.m. P -values were obtained with Student’s t-test. h Invaded LN4K1-GFP cells per high power field (HPF) at 24 h following seeding into either UF Fgn or Peak 1 Fgn alone or co-cultured with IMs with or without T101 (50 μM). FDR

    Journal: Nature Communications

    Article Title: Factor XIIIA—expressing inflammatory monocytes promote lung squamous cancer through fibrin cross-linking

    doi: 10.1038/s41467-018-04355-w

    Figure Lengend Snippet: Factor XIIIA in IMs promotes fibrin cross-linking and LUSC invasion. a Relative mRNA expression of F13a1 from sorted IMs and RMs, n = 3 mice. b Immunofluorescent (IF) imaging of IMs and RMs comparing FXIIIA (red) expression. c Dual staining for FXIIIA (red) and CD11b (green) in IMs. Contents of dotted white box are enlarged under each panel. d Confocal imaging of IMs for FXIIIA (red). White arrows point toward podosome-like structures. Scale bar: 5 μm; nuclei were stained with Hoechst (panels b – d ). e Fibrin cross-linking patterns by western blotting using a polyclonal anti-human fibrin(ogen) antibody using freshly sorted IMs and RMs (Low = 25k cells, High = 100k cells), with or without the FXIIIA-inhibitor, T101. f Percent invadopodia of LN4K1 cells growing in either unfractionated (UF Fgn, left) or Peak 1 (FXIIIA-depleted) fibrinogen (right). White arrows show evidence of invadopodia. Scale bar 50 μm. Data are averages ± s.e.m. P -values obtained with Student’s t-test. g Schematic of co-culture model (top). Representative images of LN4K1-GFP cells growing in either UF Fgn or Peak 1 with or without low (100k) or high (300k) IMs. FDR = 0.0001 for all statistical comparisons shown. Groups in e + g treated with the T101 were dosed at 50 μM. Scale bar 12.5 μm. Data are averages ± s.e.m. P -values were obtained with Student’s t-test. h Invaded LN4K1-GFP cells per high power field (HPF) at 24 h following seeding into either UF Fgn or Peak 1 Fgn alone or co-cultured with IMs with or without T101 (50 μM). FDR

    Article Snippet: Slides were incubated with primary antibody for CD11b (rabbit, 1:100, Abcam ab133357) and/or FXIII (sheep, 1:100, Enzyme Research Labs SAF13A-AP) in blocking buffer at 4 °C for 16 h. After washing cells were incubated with appropriate secondary antibodies, goat anti-rabbit (Alexa Fluor 488) and/or goat anti-sheep (Alexa Fluor 594), diluted 1:500 in blocking buffer for 1 h at RT.

    Techniques: Expressing, Mouse Assay, Imaging, Staining, Western Blot, Co-Culture Assay, Cell Culture

    Presenting melatonin at histochemical and RNA levels inhibits chronic inflammation in the lungs of mice exposed to LPS. (A–C) Significantly fewer CD45+ T cells, CD11b+ and CD11c+ and F4/80+ macrophages infiltrated into mouse lung bronchi and alveoli when LPS-exposed mice were given melatonin orally daily than non-treated mice. Luzindole (MT1/MT2 inhibitor) increased the infiltration of these inflammatory cells into the mouse lung, even when the mice were treated with melatonin. N = 5–7. (D) Mice treated with melatonin expressed lower levels of Il-6, Il-1β, Ifn-γ, and Tnf-α mRNAs as well as more Gpx, Ho-1, Sod1, and Sod2 mRNAs in the lungs than compared with LPS-exposed mice. Mice treated with luzindole (MT1/MT2 inhibitor) along with melatonin had higher levels of Il-6, Ifn-γ, and Tnf-α and decreased Gpx, Ho-1, and Sod1 mRNA expression in the lungs. N = 4–5. *p

    Journal: Frontiers in Immunology

    Article Title: An Integrative Transcriptomic and Metabolomic Study Revealed That Melatonin Plays a Protective Role in Chronic Lung Inflammation by Reducing Necroptosis

    doi: 10.3389/fimmu.2021.668002

    Figure Lengend Snippet: Presenting melatonin at histochemical and RNA levels inhibits chronic inflammation in the lungs of mice exposed to LPS. (A–C) Significantly fewer CD45+ T cells, CD11b+ and CD11c+ and F4/80+ macrophages infiltrated into mouse lung bronchi and alveoli when LPS-exposed mice were given melatonin orally daily than non-treated mice. Luzindole (MT1/MT2 inhibitor) increased the infiltration of these inflammatory cells into the mouse lung, even when the mice were treated with melatonin. N = 5–7. (D) Mice treated with melatonin expressed lower levels of Il-6, Il-1β, Ifn-γ, and Tnf-α mRNAs as well as more Gpx, Ho-1, Sod1, and Sod2 mRNAs in the lungs than compared with LPS-exposed mice. Mice treated with luzindole (MT1/MT2 inhibitor) along with melatonin had higher levels of Il-6, Ifn-γ, and Tnf-α and decreased Gpx, Ho-1, and Sod1 mRNA expression in the lungs. N = 4–5. *p

    Article Snippet: After deparaffinization and hydration, sections were incubated with primary antibodies against CD45 (1:100 dilution, ab10558, Abcam), CD11b (1:100 dilution, ab133357, Abcam), CD11c (1:100 dilution, 97585, Cell Signaling Technology), and F4/80 (1:100 dilution, ab111101, Abcam) at appropriate concentrations.

    Techniques: Mouse Assay, Expressing