anti cd11b antibody epr1344  (Abcam)

 
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    Anti CD11b antibody EPR1344
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    Abcam anti cd11b antibody epr1344
    Modulation of inflammatory cells under endotoxemic conditions. (A1) <t>CD11b-positive</t> cells were quantified as numbers of cells per high-power field. (A2) Representative images of CD11b cells in immunostained lung specimens. (B1) Iba-1 positive cells were quantified as the number of cells per high-power field. (B2) Representative images of Iba-1 in immunostained lung samples. *, P

    https://www.bioz.com/result/anti cd11b antibody epr1344/product/Abcam
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    Images

    1) Product Images from "Endothelial Glycocalyx Disorders May Be Associated With Extended Inflammation During Endotoxemia in a Diabetic Mouse Model"

    Article Title: Endothelial Glycocalyx Disorders May Be Associated With Extended Inflammation During Endotoxemia in a Diabetic Mouse Model

    Journal: Frontiers in Cell and Developmental Biology

    doi: 10.3389/fcell.2021.623582

    Modulation of inflammatory cells under endotoxemic conditions. (A1) CD11b-positive cells were quantified as numbers of cells per high-power field. (A2) Representative images of CD11b cells in immunostained lung specimens. (B1) Iba-1 positive cells were quantified as the number of cells per high-power field. (B2) Representative images of Iba-1 in immunostained lung samples. *, P
    Figure Legend Snippet: Modulation of inflammatory cells under endotoxemic conditions. (A1) CD11b-positive cells were quantified as numbers of cells per high-power field. (A2) Representative images of CD11b cells in immunostained lung specimens. (B1) Iba-1 positive cells were quantified as the number of cells per high-power field. (B2) Representative images of Iba-1 in immunostained lung samples. *, P

    Techniques Used:

    2) Product Images from "Hypoxia promotes glioma-associated macrophage infiltration via periostin and subsequent M2 polarization by upregulating TGF-beta and M-CSFR"

    Article Title: Hypoxia promotes glioma-associated macrophage infiltration via periostin and subsequent M2 polarization by upregulating TGF-beta and M-CSFR

    Journal: Oncotarget

    doi: 10.18632/oncotarget.11825

    Hypoxia, POSTN expression, TAM infiltration and the proportion of M2 subtype TAMs increased as the grade of glioma increased, and all were correlated with a worse prognosis A. IHC staining for POSTN, HIF-1α, CD11b and CD206 in four consecutive tissue slides obtained from gliomas with different grades and normal brain tissue specimens. Scale bars, 50 μm. B. A graphical analysis of (A). In all, 47.8% of the glioma cases showed POSTN+ and HIF-1α+ staining, and 16.9% and 15.5% of the GBM cases showed single-positive cells that were POSTN+/HIF-1α- or POSTN-/HIF-1α+, respectively. Only 19.8% of the cases showed both types of negative staining. C. Immunofluorescence staining for the TAM marker CD11b (green) and the M2 type TAM marker CD206 (red). D. A graphical analysis of figure (C) showing that TAM infiltration and the proportion of M2 type cells increased as the grade of the glioma increased. TAM density was analyzed using ImageJ. *, P
    Figure Legend Snippet: Hypoxia, POSTN expression, TAM infiltration and the proportion of M2 subtype TAMs increased as the grade of glioma increased, and all were correlated with a worse prognosis A. IHC staining for POSTN, HIF-1α, CD11b and CD206 in four consecutive tissue slides obtained from gliomas with different grades and normal brain tissue specimens. Scale bars, 50 μm. B. A graphical analysis of (A). In all, 47.8% of the glioma cases showed POSTN+ and HIF-1α+ staining, and 16.9% and 15.5% of the GBM cases showed single-positive cells that were POSTN+/HIF-1α- or POSTN-/HIF-1α+, respectively. Only 19.8% of the cases showed both types of negative staining. C. Immunofluorescence staining for the TAM marker CD11b (green) and the M2 type TAM marker CD206 (red). D. A graphical analysis of figure (C) showing that TAM infiltration and the proportion of M2 type cells increased as the grade of the glioma increased. TAM density was analyzed using ImageJ. *, P

    Techniques Used: Expressing, Immunohistochemistry, Staining, Negative Staining, Immunofluorescence, Marker

    3) Product Images from "A novel neural stem cell-derived immunocompetent mouse model of glioblastoma for preclinical studies"

    Article Title: A novel neural stem cell-derived immunocompetent mouse model of glioblastoma for preclinical studies

    Journal: bioRxiv

    doi: 10.1101/2020.03.16.993196

    The novel cell lines give rise to orthotopic tumors with characteristics of human glioblastomas a,b GFP-Immunofluorescence staining (green) of tNSC3(a) and mGB2 (b) orthotopic tumors. Cellular nuclei are stained with DAPI and pseudocolored in blue. Scale bars, 1000 μm. Dotted lines show tumor area. N indicates a necrotic area in the mGB2 orthotopic glioma. c,d Zoom-in of images from a and b respectively showing area at the tumor border. T indicates tumor area delineated by dotted lines. Arrows denote GFP-positive glioma cells invading the surrounding normal brain parenchyma. e-h Histopathological features of orthotopic tNSC3 (e,g) and mGB2 (f,h) gliomas. Sections were stained with hematoxylin and eosin (H E). Arrows in e,f denote areas of microvascular proliferation; arrows in g,h indicate mitotic figures. i,j Ki67 expression (purple) in orthotopic tNSC3 (e) and mGB2 (f) gliomas detected by immunohistochemistry. The sections were counterstained with hematoxylin. k-r Immunofluorescence staining for Olig2 (k,l), Gfap (m,n), Cd11b (o,p), Iba1 (q,r) within tumor areas from orthotopic tNSC3 (I,k,m,o) and mGB2 (j,l,n,p) gliomas. Cellular nuclei are stained with DAPI and pseudocolored in blue.
    Figure Legend Snippet: The novel cell lines give rise to orthotopic tumors with characteristics of human glioblastomas a,b GFP-Immunofluorescence staining (green) of tNSC3(a) and mGB2 (b) orthotopic tumors. Cellular nuclei are stained with DAPI and pseudocolored in blue. Scale bars, 1000 μm. Dotted lines show tumor area. N indicates a necrotic area in the mGB2 orthotopic glioma. c,d Zoom-in of images from a and b respectively showing area at the tumor border. T indicates tumor area delineated by dotted lines. Arrows denote GFP-positive glioma cells invading the surrounding normal brain parenchyma. e-h Histopathological features of orthotopic tNSC3 (e,g) and mGB2 (f,h) gliomas. Sections were stained with hematoxylin and eosin (H E). Arrows in e,f denote areas of microvascular proliferation; arrows in g,h indicate mitotic figures. i,j Ki67 expression (purple) in orthotopic tNSC3 (e) and mGB2 (f) gliomas detected by immunohistochemistry. The sections were counterstained with hematoxylin. k-r Immunofluorescence staining for Olig2 (k,l), Gfap (m,n), Cd11b (o,p), Iba1 (q,r) within tumor areas from orthotopic tNSC3 (I,k,m,o) and mGB2 (j,l,n,p) gliomas. Cellular nuclei are stained with DAPI and pseudocolored in blue.

    Techniques Used: Immunofluorescence, Staining, Expressing, Immunohistochemistry

    4) Product Images from "LRP1 deficiency in microglia blocks neuro-inflammation in the spinal dorsal horn and neuropathic pain processing"

    Article Title: LRP1 deficiency in microglia blocks neuro-inflammation in the spinal dorsal horn and neuropathic pain processing

    Journal: Glia

    doi: 10.1002/glia.23599

    TAM-induced LRP1 deficiency in microglia does not alter myeloid cell infiltration or inflammation in injured sciatic nerves. ( a ) TAM-treated Cx3cr1- CreER T -LRP1 fl/fl (LRP1 fl/fl ) mice and Cx3cr1- CreER T -LRP1 ( LRP1 ) mice were subjected to PNL or sham-operation. Sciatic nerve tissue distal to the injury site was harvested 3 days later. The area of the nerve directly downstream of the ligation was immunostained to detect the myeloid cell marker CD11b. Images represent n = 3 sham-operated animals and 4 mice subjected to PNL for each genotype. ( b ) The number of CD11b-positive cells present in the nerves was counted. Although PNL significantly increased the number of cells, there was no change with mouse genotype (mean ± s.e.m.; n = 3 sham-operated animals and n = 4 mice subjected to PNL; *** p
    Figure Legend Snippet: TAM-induced LRP1 deficiency in microglia does not alter myeloid cell infiltration or inflammation in injured sciatic nerves. ( a ) TAM-treated Cx3cr1- CreER T -LRP1 fl/fl (LRP1 fl/fl ) mice and Cx3cr1- CreER T -LRP1 ( LRP1 ) mice were subjected to PNL or sham-operation. Sciatic nerve tissue distal to the injury site was harvested 3 days later. The area of the nerve directly downstream of the ligation was immunostained to detect the myeloid cell marker CD11b. Images represent n = 3 sham-operated animals and 4 mice subjected to PNL for each genotype. ( b ) The number of CD11b-positive cells present in the nerves was counted. Although PNL significantly increased the number of cells, there was no change with mouse genotype (mean ± s.e.m.; n = 3 sham-operated animals and n = 4 mice subjected to PNL; *** p

    Techniques Used: Mouse Assay, Ligation, Marker

    5) Product Images from "An Integrative Transcriptomic and Metabolomic Study Revealed That Melatonin Plays a Protective Role in Chronic Lung Inflammation by Reducing Necroptosis"

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

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2021.668002

    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
    Figure Legend 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

    Techniques Used: Mouse Assay, Expressing

    6) Product Images from "Schistosoma mansoni Coinfection Attenuates Murine Toxoplasma gondii-Induced Crohn's-Like Ileitis by Preserving the Epithelial Barrier and Downregulating the Inflammatory Response"

    Article Title: Schistosoma mansoni Coinfection Attenuates Murine Toxoplasma gondii-Induced Crohn's-Like Ileitis by Preserving the Epithelial Barrier and Downregulating the Inflammatory Response

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2019.00442

    T. gondii -induced ileitis is characterized by an intense inflammatory cell infiltration in the lamina propria, including CD4- and CD11b-positive cells. Prior S. mansoni infection attenuates T. gondii -induced accumulation of CD4- (A) and CD11b-positive cells (B) . The horizontal bars represent the medians, the boxes represent the 25th and 75th percentiles, and the vertical lines below and above the boxes represent the minimum and maximum values, respectively. The analysis was performed by Kruskal-Wallis ANOVA on ranks test, in which multiple comparisons were carried out using the Dunnett's test. The scale bars represent 20 μm. The data are representative of three independent experiments, with 5–7 animals per group.
    Figure Legend Snippet: T. gondii -induced ileitis is characterized by an intense inflammatory cell infiltration in the lamina propria, including CD4- and CD11b-positive cells. Prior S. mansoni infection attenuates T. gondii -induced accumulation of CD4- (A) and CD11b-positive cells (B) . The horizontal bars represent the medians, the boxes represent the 25th and 75th percentiles, and the vertical lines below and above the boxes represent the minimum and maximum values, respectively. The analysis was performed by Kruskal-Wallis ANOVA on ranks test, in which multiple comparisons were carried out using the Dunnett's test. The scale bars represent 20 μm. The data are representative of three independent experiments, with 5–7 animals per group.

    Techniques Used: Infection

    7) Product Images from "Vitamin D upregulates the macrophage complement receptor immunoglobulin in innate immunity to microbial pathogens"

    Article Title: Vitamin D upregulates the macrophage complement receptor immunoglobulin in innate immunity to microbial pathogens

    Journal: Communications Biology

    doi: 10.1038/s42003-021-01943-3

    Effect of 1,25D on macrophage CR3 and CR4 expression and phagocytosis. Monocytes were cultured for either 3 days (for mRNA expression) or 5 days (for protein expression) with 1,25D and examined for complement receptor expression. Relative expression (RE) of mRNA or protein was measured against GAPDH. a Macrophages were examined for CD11b and CD11c mRNA expression. Data are expressed as fold-change compared with untreated control from three experiments each conducted with cells from a different individual and expressed as mean ± s.d. b Macrophages were examined for CD11c and CD11b protein expression by western blotting, normalized against GAPDH from four experiments each with cells from a different individual. Representative western blots are shown. c Macrophages were analysed for CD11b and CD11c surface expression by flow cytometry. The PE MFI values are shown of four (CD11b) and three (CD11c) experiments, each conducted with cells from a different individual. d Phagocytosis of S. aureus bioparticles by macrophages as measured by the pH-sensitive pHrodo™ Red dye. Data are expressed as MFI, each conducted with cells from a different individual. e Phagocytosis of opsonized C. albicans by macrophages derived from monocytes cultured in either the presence or absence of 100 nM 1,25D for 5 days, is expressed as the number of engulfed particles per cell (left graph) and the percentage of cells with four or more phagocytosed particles (right graph). Data are presented as mean ± s.d. of three experiments each with cells from a different individual. a , b Data are presented as mean ± s.d. P values were calculated using one-way ANOVA followed by Dunnett’s multiple comparison test. c – e P values were calculated using paired two-tailed ( c ) or one-tailed ( d , e ) Student’s t -test. Significance of differences between 1,25D versus control, * P
    Figure Legend Snippet: Effect of 1,25D on macrophage CR3 and CR4 expression and phagocytosis. Monocytes were cultured for either 3 days (for mRNA expression) or 5 days (for protein expression) with 1,25D and examined for complement receptor expression. Relative expression (RE) of mRNA or protein was measured against GAPDH. a Macrophages were examined for CD11b and CD11c mRNA expression. Data are expressed as fold-change compared with untreated control from three experiments each conducted with cells from a different individual and expressed as mean ± s.d. b Macrophages were examined for CD11c and CD11b protein expression by western blotting, normalized against GAPDH from four experiments each with cells from a different individual. Representative western blots are shown. c Macrophages were analysed for CD11b and CD11c surface expression by flow cytometry. The PE MFI values are shown of four (CD11b) and three (CD11c) experiments, each conducted with cells from a different individual. d Phagocytosis of S. aureus bioparticles by macrophages as measured by the pH-sensitive pHrodo™ Red dye. Data are expressed as MFI, each conducted with cells from a different individual. e Phagocytosis of opsonized C. albicans by macrophages derived from monocytes cultured in either the presence or absence of 100 nM 1,25D for 5 days, is expressed as the number of engulfed particles per cell (left graph) and the percentage of cells with four or more phagocytosed particles (right graph). Data are presented as mean ± s.d. of three experiments each with cells from a different individual. a , b Data are presented as mean ± s.d. P values were calculated using one-way ANOVA followed by Dunnett’s multiple comparison test. c – e P values were calculated using paired two-tailed ( c ) or one-tailed ( d , e ) Student’s t -test. Significance of differences between 1,25D versus control, * P

    Techniques Used: Expressing, Cell Culture, Western Blot, Flow Cytometry, Derivative Assay, Two Tailed Test, One-tailed Test

    8) Product Images from "Pancreatitis severity in mice with impaired CFTR function but pancreatic sufficiency is mediated via ductal and inflammatory cells‐Not acinar cells, et al. Pancreatitis severity in mice with impaired CFTR function but pancreatic sufficiency is mediated via ductal and inflammatory cells‐Not acinar cells"

    Article Title: Pancreatitis severity in mice with impaired CFTR function but pancreatic sufficiency is mediated via ductal and inflammatory cells‐Not acinar cells, et al. Pancreatitis severity in mice with impaired CFTR function but pancreatic sufficiency is mediated via ductal and inflammatory cells‐Not acinar cells

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/jcmm.16404

    Histological damage was increased in CFTR transgenic mice as shown by haematoxylin and eosin stainings (A). The calibration bar represents 100 µm. (A) Quantification of histological changes was performed by a separate evaluation of necrosis, inflammation and pancreatic oedema (B). Summed up, there was a significant increase of pancreatic damage at 8h after induction of pancreatitis in the CFTR transgenic animals, seen by a higher histology score (B). The single parameters showed a clear trend towards an increase but only the quantification of the infiltrating leucocytes reached significance 8h after the onset of the disease (C), and still showed a trend at 24 h. A detailed analysis of infiltrating leucocytes by immunohistochemical staining of CD11b and p67‐phox showed a prominent infiltration of CD11b + macrophages in both mice strains at 8h after induction of pancreatitis that was more predominant in the CFTR tm1HGU mice (D). In contrast to CD11b + macrophages, p67‐phox‐positive neutrophils could rarely be observed (E). At least five mice were used in every group. The experiments were performed in triplicates. Asterisks indicate significant differences with P
    Figure Legend Snippet: Histological damage was increased in CFTR transgenic mice as shown by haematoxylin and eosin stainings (A). The calibration bar represents 100 µm. (A) Quantification of histological changes was performed by a separate evaluation of necrosis, inflammation and pancreatic oedema (B). Summed up, there was a significant increase of pancreatic damage at 8h after induction of pancreatitis in the CFTR transgenic animals, seen by a higher histology score (B). The single parameters showed a clear trend towards an increase but only the quantification of the infiltrating leucocytes reached significance 8h after the onset of the disease (C), and still showed a trend at 24 h. A detailed analysis of infiltrating leucocytes by immunohistochemical staining of CD11b and p67‐phox showed a prominent infiltration of CD11b + macrophages in both mice strains at 8h after induction of pancreatitis that was more predominant in the CFTR tm1HGU mice (D). In contrast to CD11b + macrophages, p67‐phox‐positive neutrophils could rarely be observed (E). At least five mice were used in every group. The experiments were performed in triplicates. Asterisks indicate significant differences with P

    Techniques Used: Transgenic Assay, Mouse Assay, Immunohistochemistry, Staining

    Related Articles

    Incubation:

    Article Title: miR-143/145 differentially regulate hematopoietic stem and progenitor activity through suppression of canonical TGFβ signaling
    Article Snippet: Alternatively, freshly cut tissues were analyzed for CD11b expression and immunohistochemistry was performed using the Ventana DiscoveryXT platform. .. In brief, tissue sections were incubated in Tris EDTA buffer at 95 °C to retrieve antigenicity, followed by incubation with the anti-CD11b primary antibody (ab133357, Abcam). .. Bound antibodies were incubated with secondary horse radish peroxidase-conjugated antibodies which was followed by Chromomap DAB detection.

    Article Title: IL-11 induces differentiation of myeloid-derived suppressor cells through activation of STAT3 signalling pathway
    Article Snippet: .. Endogenous peroxidase activity was blocked with 0.3% H2 O2 at room temperature for 10 min. After protein blocking at room temperature for 10 min, slides were incubated with a polyclonal rabbit anti-human IL-11 (RPA057Hu01, Uscn Life Science, USA), a polyclonal rabbit anti-human phospho-STAT3 (Tyr705) antibody (9145, Cell Signaling Technology), a monoclonal mouse anit-CD14 antibody (MY4), or a rabbit monoclonal anti-CD11b antibody (EPR1344, Abcam, Cambridge, UK) overnight at 4 °C. .. Sections were then incubated at room temperature for 15 min with a horseradish peroxidase-labelled anti-rabbit Igs.

    Article Title: Endothelial Glycocalyx Disorders May Be Associated With Extended Inflammation During Endotoxemia in a Diabetic Mouse Model
    Article Snippet: .. Immunohistochemistry Lung sections were incubated with primary antibodies against the neutrophil and macrophage surface marker CD11b (ab133357; Abcam, Cambridge, United Kingdom), the vascular endothelial cell marker CD31 (DIO-310; Dianova GmbH, Hamburg, Germany), and the activated macrophage surface marker Iba-1 (019-19741; Wako Pure Chemical, Osaka, Japan). .. Sections were immunostained with the Vectastain Elite ABC system (Vector Laboratories, Burlingame, CA, United States) as previously described ( ).

    Activity Assay:

    Article Title: IL-11 induces differentiation of myeloid-derived suppressor cells through activation of STAT3 signalling pathway
    Article Snippet: .. Endogenous peroxidase activity was blocked with 0.3% H2 O2 at room temperature for 10 min. After protein blocking at room temperature for 10 min, slides were incubated with a polyclonal rabbit anti-human IL-11 (RPA057Hu01, Uscn Life Science, USA), a polyclonal rabbit anti-human phospho-STAT3 (Tyr705) antibody (9145, Cell Signaling Technology), a monoclonal mouse anit-CD14 antibody (MY4), or a rabbit monoclonal anti-CD11b antibody (EPR1344, Abcam, Cambridge, UK) overnight at 4 °C. .. Sections were then incubated at room temperature for 15 min with a horseradish peroxidase-labelled anti-rabbit Igs.

    Blocking Assay:

    Article Title: IL-11 induces differentiation of myeloid-derived suppressor cells through activation of STAT3 signalling pathway
    Article Snippet: .. Endogenous peroxidase activity was blocked with 0.3% H2 O2 at room temperature for 10 min. After protein blocking at room temperature for 10 min, slides were incubated with a polyclonal rabbit anti-human IL-11 (RPA057Hu01, Uscn Life Science, USA), a polyclonal rabbit anti-human phospho-STAT3 (Tyr705) antibody (9145, Cell Signaling Technology), a monoclonal mouse anit-CD14 antibody (MY4), or a rabbit monoclonal anti-CD11b antibody (EPR1344, Abcam, Cambridge, UK) overnight at 4 °C. .. Sections were then incubated at room temperature for 15 min with a horseradish peroxidase-labelled anti-rabbit Igs.

    Immunohistochemistry:

    Article Title: Endothelial Glycocalyx Disorders May Be Associated With Extended Inflammation During Endotoxemia in a Diabetic Mouse Model
    Article Snippet: .. Immunohistochemistry Lung sections were incubated with primary antibodies against the neutrophil and macrophage surface marker CD11b (ab133357; Abcam, Cambridge, United Kingdom), the vascular endothelial cell marker CD31 (DIO-310; Dianova GmbH, Hamburg, Germany), and the activated macrophage surface marker Iba-1 (019-19741; Wako Pure Chemical, Osaka, Japan). .. Sections were immunostained with the Vectastain Elite ABC system (Vector Laboratories, Burlingame, CA, United States) as previously described ( ).

    Marker:

    Article Title: Endothelial Glycocalyx Disorders May Be Associated With Extended Inflammation During Endotoxemia in a Diabetic Mouse Model
    Article Snippet: .. Immunohistochemistry Lung sections were incubated with primary antibodies against the neutrophil and macrophage surface marker CD11b (ab133357; Abcam, Cambridge, United Kingdom), the vascular endothelial cell marker CD31 (DIO-310; Dianova GmbH, Hamburg, Germany), and the activated macrophage surface marker Iba-1 (019-19741; Wako Pure Chemical, Osaka, Japan). .. Sections were immunostained with the Vectastain Elite ABC system (Vector Laboratories, Burlingame, CA, United States) as previously described ( ).

    Staining:

    Article Title: Blood coagulation factor XII drives adaptive immunity during neuroinflammation via CD87-mediated modulation of dendritic cells
    Article Snippet: Sections were stained with the primary antibodies to the following: FXII (1:50, Proteintech), human CD11c (1:100, clone 3.9, Abcam, Cambridge, UK), human albumin (1:50, Origene Technologies, Rockville, MD, USA), ionized calcium-binding adapter molecule 1 (1:250, polyclonal, Wako Chemicals GmbH, Neuss, Germany), glial fibrillary acidic protein (GFAP; 1:1,000, clone G-A-5, Sigma-Aldrich) and mouse CD11c (1:1,000, clone N418, eBioscience, San Diego, CA, USA). .. Astrocyte and microglia cultures were stained with anti-GFAP and anti-CD11b (1:1,000, clone EPR1344, Abcam), respectively. .. In addition, both were stained with anti-MHC-I (1:200, clone ER-HR52, Abcam) and anti-MHC-II (1:50, clone NIMR-4, Abcam).

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    Abcam anti cd11b
    FXII favours the emergence of T H 17 cells via DC. ( a ) Real-time reverse transcription–PCR (rRT–PCR) analyses for Cd87 gene expression in CD4 + , CD8 + and B220 + cells isolated from lymphocytes as well as in <t>CD11b</t> + and CD11c + cells isolated from spleens of naive WT mice. ( b ) rRT–PCR analyses for Cd87 gene expression in CD4 + CD25 − (Crtl) and CD4 + CD25 + (T reg ) cells isolated from lymph nodes under basal conditions or after a 48-h incubation with antibodies against CD3 and CD28 under neutral conditions (T H 0) or in the presence of the appropriate cytokine and neutralizing antibody mixtures for differentiation into T H 1 or T H 17 cells as well as in splenic cDCs or pDCs. ( c ) Flow cytometry analysis for CD87 expression in cDCs (stained with CD11c, left panel) and pDCs (stained with CD317, right panel) isolated from the spleen under basal conditions or after a 24-h stimulation with 1 μg ml −1 LPS or 10 μg ml −1 CpG oligodeoxynucleotide 1,826, respectively. For cDCs and pDCs, representative dot plots for CD87 expression are shown. ( d ) rRT–PCR analyses for Par1 , Par2 , Par3 , Par4 and Cd87 expression in cDCs and pDCs isolated from the spleen. ( e ) Splenic cDCs and pDCs from WT animals were incubated with medium only (Ctrl) or stimulated with 1 μg ml −1 LPS (for cDCs) or with 10 μg ml −1 CpG oligodeoxynucleotide 1,826 (for pDCs) in the absence or presence of 60 nM FXII, respectively. After 48 h, cytokine concentrations were measured in culture supernatants. In a , b and d , data are given as mean±s.e.m. of three independent experiments and presented as fold change in transcript expression relative to 18S rRNA. In c and e , data are given as mean±s.e.m. of three independent experiments, each performed in triplicate (non-parametric Mann–Whitney U -test). * P
    Anti Cd11b, supplied by Abcam, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    FXII favours the emergence of T H 17 cells via DC. ( a ) Real-time reverse transcription–PCR (rRT–PCR) analyses for Cd87 gene expression in CD4 + , CD8 + and B220 + cells isolated from lymphocytes as well as in CD11b + and CD11c + cells isolated from spleens of naive WT mice. ( b ) rRT–PCR analyses for Cd87 gene expression in CD4 + CD25 − (Crtl) and CD4 + CD25 + (T reg ) cells isolated from lymph nodes under basal conditions or after a 48-h incubation with antibodies against CD3 and CD28 under neutral conditions (T H 0) or in the presence of the appropriate cytokine and neutralizing antibody mixtures for differentiation into T H 1 or T H 17 cells as well as in splenic cDCs or pDCs. ( c ) Flow cytometry analysis for CD87 expression in cDCs (stained with CD11c, left panel) and pDCs (stained with CD317, right panel) isolated from the spleen under basal conditions or after a 24-h stimulation with 1 μg ml −1 LPS or 10 μg ml −1 CpG oligodeoxynucleotide 1,826, respectively. For cDCs and pDCs, representative dot plots for CD87 expression are shown. ( d ) rRT–PCR analyses for Par1 , Par2 , Par3 , Par4 and Cd87 expression in cDCs and pDCs isolated from the spleen. ( e ) Splenic cDCs and pDCs from WT animals were incubated with medium only (Ctrl) or stimulated with 1 μg ml −1 LPS (for cDCs) or with 10 μg ml −1 CpG oligodeoxynucleotide 1,826 (for pDCs) in the absence or presence of 60 nM FXII, respectively. After 48 h, cytokine concentrations were measured in culture supernatants. In a , b and d , data are given as mean±s.e.m. of three independent experiments and presented as fold change in transcript expression relative to 18S rRNA. In c and e , data are given as mean±s.e.m. of three independent experiments, each performed in triplicate (non-parametric Mann–Whitney U -test). * P

    Journal: Nature Communications

    Article Title: Blood coagulation factor XII drives adaptive immunity during neuroinflammation via CD87-mediated modulation of dendritic cells

    doi: 10.1038/ncomms11626

    Figure Lengend Snippet: FXII favours the emergence of T H 17 cells via DC. ( a ) Real-time reverse transcription–PCR (rRT–PCR) analyses for Cd87 gene expression in CD4 + , CD8 + and B220 + cells isolated from lymphocytes as well as in CD11b + and CD11c + cells isolated from spleens of naive WT mice. ( b ) rRT–PCR analyses for Cd87 gene expression in CD4 + CD25 − (Crtl) and CD4 + CD25 + (T reg ) cells isolated from lymph nodes under basal conditions or after a 48-h incubation with antibodies against CD3 and CD28 under neutral conditions (T H 0) or in the presence of the appropriate cytokine and neutralizing antibody mixtures for differentiation into T H 1 or T H 17 cells as well as in splenic cDCs or pDCs. ( c ) Flow cytometry analysis for CD87 expression in cDCs (stained with CD11c, left panel) and pDCs (stained with CD317, right panel) isolated from the spleen under basal conditions or after a 24-h stimulation with 1 μg ml −1 LPS or 10 μg ml −1 CpG oligodeoxynucleotide 1,826, respectively. For cDCs and pDCs, representative dot plots for CD87 expression are shown. ( d ) rRT–PCR analyses for Par1 , Par2 , Par3 , Par4 and Cd87 expression in cDCs and pDCs isolated from the spleen. ( e ) Splenic cDCs and pDCs from WT animals were incubated with medium only (Ctrl) or stimulated with 1 μg ml −1 LPS (for cDCs) or with 10 μg ml −1 CpG oligodeoxynucleotide 1,826 (for pDCs) in the absence or presence of 60 nM FXII, respectively. After 48 h, cytokine concentrations were measured in culture supernatants. In a , b and d , data are given as mean±s.e.m. of three independent experiments and presented as fold change in transcript expression relative to 18S rRNA. In c and e , data are given as mean±s.e.m. of three independent experiments, each performed in triplicate (non-parametric Mann–Whitney U -test). * P

    Article Snippet: Astrocyte and microglia cultures were stained with anti-GFAP and anti-CD11b (1:1,000, clone EPR1344, Abcam), respectively.

    Techniques: Polymerase Chain Reaction, Quantitative RT-PCR, Expressing, Isolation, Mouse Assay, Incubation, Flow Cytometry, Staining, MANN-WHITNEY

    Factor XII deficiency alters T-cell differentiation. ( a ) Tbx21 , Gata3 , Rorc and Foxp3 expression from LN cells at day 10 ( d 10 ) or d max as well as from brain-infiltrating leukocytes (BILs) at d max after MOG 35–55 immunization is determined by real-time reverse transcription–PCR using 18S rRNA for normalization. Data (mean±s.e.m. of five experiments) are given as fold change in normalized gene expression in animals relative to WT controls. ( b ) At d 10 after MOG 35–55 immunization, proliferation and cytokine production by CD4 + T cells purified from LN and restimulated with 10 μg ml −1 MOG 35–55 and irradiated (35 Gy) antigen-presenting cells in vitro for 48 h (upper panels), and by CD11c + DCs purified from spleens and incubated with 1 μg ml −1 LPS in vitro for 48 h (lower panels) are shown. ( c ) Mononuclear cells were isolated from the LN of WT and F12 −/− animals at d 10 post induction of EAE. Cells were polyclonal restimulated in vitro , stained with anti-CD3 and anti-CD4, fixed and permeabilized, stained intracellularly with anti-IL-17A and analysed by flow cytometry for the percentage of IL-17A-producing CD4 + T cells. ( d ) Cytokine production by purified BILs from MOG 35–55 -immunized WT or F12 −/− mice at d max after restimulation with 10 μg ml −1 MOG 35–55 for 48 h. ( e , f ) BILs and LNs were isolated from WT and F12 −/− animals at d max post induction of EAE and polyclonal restimulated in vitro . For the detection of the percentage of IL-17A-producing lymphocytes (CD45 high CD11b neg cells or CD4 + CD3 + T cells), BILs or LNs were stained with anti-CD11b and anti-CD45, or anti-CD3 and anti-CD4, fixed and permeabilized, stained intracellularly with anti-IL-17A and analysed by flow cytometry. In b – f , data are given as means±s.e.m. of three independent experiments, each performed in triplicate. For c , e and f , representative dot plots for IL-17A expression are shown. For a – f , non-parametric Mann–Whitney U -test. * P

    Journal: Nature Communications

    Article Title: Blood coagulation factor XII drives adaptive immunity during neuroinflammation via CD87-mediated modulation of dendritic cells

    doi: 10.1038/ncomms11626

    Figure Lengend Snippet: Factor XII deficiency alters T-cell differentiation. ( a ) Tbx21 , Gata3 , Rorc and Foxp3 expression from LN cells at day 10 ( d 10 ) or d max as well as from brain-infiltrating leukocytes (BILs) at d max after MOG 35–55 immunization is determined by real-time reverse transcription–PCR using 18S rRNA for normalization. Data (mean±s.e.m. of five experiments) are given as fold change in normalized gene expression in animals relative to WT controls. ( b ) At d 10 after MOG 35–55 immunization, proliferation and cytokine production by CD4 + T cells purified from LN and restimulated with 10 μg ml −1 MOG 35–55 and irradiated (35 Gy) antigen-presenting cells in vitro for 48 h (upper panels), and by CD11c + DCs purified from spleens and incubated with 1 μg ml −1 LPS in vitro for 48 h (lower panels) are shown. ( c ) Mononuclear cells were isolated from the LN of WT and F12 −/− animals at d 10 post induction of EAE. Cells were polyclonal restimulated in vitro , stained with anti-CD3 and anti-CD4, fixed and permeabilized, stained intracellularly with anti-IL-17A and analysed by flow cytometry for the percentage of IL-17A-producing CD4 + T cells. ( d ) Cytokine production by purified BILs from MOG 35–55 -immunized WT or F12 −/− mice at d max after restimulation with 10 μg ml −1 MOG 35–55 for 48 h. ( e , f ) BILs and LNs were isolated from WT and F12 −/− animals at d max post induction of EAE and polyclonal restimulated in vitro . For the detection of the percentage of IL-17A-producing lymphocytes (CD45 high CD11b neg cells or CD4 + CD3 + T cells), BILs or LNs were stained with anti-CD11b and anti-CD45, or anti-CD3 and anti-CD4, fixed and permeabilized, stained intracellularly with anti-IL-17A and analysed by flow cytometry. In b – f , data are given as means±s.e.m. of three independent experiments, each performed in triplicate. For c , e and f , representative dot plots for IL-17A expression are shown. For a – f , non-parametric Mann–Whitney U -test. * P

    Article Snippet: Astrocyte and microglia cultures were stained with anti-GFAP and anti-CD11b (1:1,000, clone EPR1344, Abcam), respectively.

    Techniques: Cell Differentiation, Expressing, Polymerase Chain Reaction, Purification, Irradiation, In Vitro, Incubation, Isolation, Staining, Flow Cytometry, Mouse Assay, MANN-WHITNEY

    FXII influences DCs in the CNS. ( a ) EAE development is shown in WT mice after adoptive transfer of CD4 + lymphocytes and CD11c + cells isolated from WT or Cd87 −/− mice on day 12 post immunization and restimulated with 10 μg ml −1 MOG 35–55 and 0.5 ng ml −1 IL-12 with or without 60 nM FXII for 72 h. Mean clinical and mean cumulative scores±s.e.m. over time of three independent experiments are given (non-parametric Mann–Whitney U -test). ( b ) BM chimeras were created by transferring WT and Cd87 −/− BM into WT and Cd87 −/− recipient mice after radiation. Mean clinical and mean cumulative scores±s.e.m. of EAE from three independent experiments are shown (non-parametric Mann–Whitney U -test). ( c , d ) Brain-infiltrating leukocytes (BILs) were separated into cDC + and cDC − by sorting via flow cytometry based on indicated surface markers at d max after EAE induction. Both subsets from WT or F12 –/– mice were analysed for Il-6 expression by real-time reverse transcription–PCR using 18s rRNA for normalization. Data are given as mean±s.e.m. of two experiments, each experiment generated from pooled brain and spinal-cord-derived cells of n =6–7 mice per group and presented as fold change in normalized gene expression relative to WT controls. ( e ) Flow cytometric analysis of BILs from WT and F12 −/− animals at d max after EAE induction determined the expression of CD80, CD86 and MHC-II in cDCs that were pre-gated for CD45 high CD11b + CD11c + cells. Data are representative of two independent experiments with four mice per genotype. ( f ) Histological analysis of spinal cord sections stained for the nucleus (4,6-diamidino-2-phenylindole (DAPI), blue), FXII (red) and CD11c (green) from the lumbar region of EAE WT animals at d max . Scale bar, 100 μm. * P

    Journal: Nature Communications

    Article Title: Blood coagulation factor XII drives adaptive immunity during neuroinflammation via CD87-mediated modulation of dendritic cells

    doi: 10.1038/ncomms11626

    Figure Lengend Snippet: FXII influences DCs in the CNS. ( a ) EAE development is shown in WT mice after adoptive transfer of CD4 + lymphocytes and CD11c + cells isolated from WT or Cd87 −/− mice on day 12 post immunization and restimulated with 10 μg ml −1 MOG 35–55 and 0.5 ng ml −1 IL-12 with or without 60 nM FXII for 72 h. Mean clinical and mean cumulative scores±s.e.m. over time of three independent experiments are given (non-parametric Mann–Whitney U -test). ( b ) BM chimeras were created by transferring WT and Cd87 −/− BM into WT and Cd87 −/− recipient mice after radiation. Mean clinical and mean cumulative scores±s.e.m. of EAE from three independent experiments are shown (non-parametric Mann–Whitney U -test). ( c , d ) Brain-infiltrating leukocytes (BILs) were separated into cDC + and cDC − by sorting via flow cytometry based on indicated surface markers at d max after EAE induction. Both subsets from WT or F12 –/– mice were analysed for Il-6 expression by real-time reverse transcription–PCR using 18s rRNA for normalization. Data are given as mean±s.e.m. of two experiments, each experiment generated from pooled brain and spinal-cord-derived cells of n =6–7 mice per group and presented as fold change in normalized gene expression relative to WT controls. ( e ) Flow cytometric analysis of BILs from WT and F12 −/− animals at d max after EAE induction determined the expression of CD80, CD86 and MHC-II in cDCs that were pre-gated for CD45 high CD11b + CD11c + cells. Data are representative of two independent experiments with four mice per genotype. ( f ) Histological analysis of spinal cord sections stained for the nucleus (4,6-diamidino-2-phenylindole (DAPI), blue), FXII (red) and CD11c (green) from the lumbar region of EAE WT animals at d max . Scale bar, 100 μm. * P

    Article Snippet: Astrocyte and microglia cultures were stained with anti-GFAP and anti-CD11b (1:1,000, clone EPR1344, Abcam), respectively.

    Techniques: Mouse Assay, Adoptive Transfer Assay, Isolation, MANN-WHITNEY, Transferring, Flow Cytometry, Expressing, Polymerase Chain Reaction, Generated, Derivative Assay, Staining

    FXII controls cytokine production via CD87. ( a ) Splenic cDCs from naive WT animals were stimulated with 1 μg ml −1 LPS in the absence and presence of 60 nM activated FXII (FXIIa). After 48 h, cytokine concentrations were measured in culture supernatants by ELISA. ( b ) Cytokine production of splenic cDCs from WT animals stimulated with 1 μg ml −1 LPS in the absence and presence of 60 nM non-cleavable FXII. After 48 h, cytokine concentrations were determined in culture supernatants by ELISA. ( c ) Cytokine production of splenic cDCs from CD87-deficient ( Cd87 −/− ) mice stimulated with 1 μg ml −1 LPS alone or in the absence and presence of 60 nM FXII for 48 h. ( d ) Cytokine production of splenic cDCs from CD11b-deficient ( Itgam −/− ) animals stimulated with 1 μg ml −1 LPS in the absence and presence of 60 nM FXII for 48 h. ( e ) Cytosolic cAMP formation measured in cDCs from WT or Cd87 −/− mice that were incubated with medium only (Ctrl) or stimulated with 1 μg ml −1 LPS for 10 min in the absence (Ctrl) or presence of 60 nM FXII. ( f ) Cytokine concentrations of IL-6 (left panel) and IL-23 (right panel) in the supernatants of WT cDCs stimulated with 1 μg ml −1 LPS or 60 nM FXII for 48 h in the presence of protein kinase A inhibitors (3 μM H-89 and 100 μM Rp-8-Br-cAMP). ( g ) Cytokine concentrations of IFN-γ, IL-17A, IL-6, IL-12 and IL-23 were measured in the supernatants from co-cultures of CD4 + T lymphocytes from WT (upper panel) or Cd87 −/− (lower panel) that were polyclonal activated together with cDCs from WT and Cd87 −/− in the absence or presence of 60 nM FXII. In a – g , data are given as means±s.e.m. of three independent experiments, each performed in duplicate (non-parametric Mann–Whitney U -test). * P

    Journal: Nature Communications

    Article Title: Blood coagulation factor XII drives adaptive immunity during neuroinflammation via CD87-mediated modulation of dendritic cells

    doi: 10.1038/ncomms11626

    Figure Lengend Snippet: FXII controls cytokine production via CD87. ( a ) Splenic cDCs from naive WT animals were stimulated with 1 μg ml −1 LPS in the absence and presence of 60 nM activated FXII (FXIIa). After 48 h, cytokine concentrations were measured in culture supernatants by ELISA. ( b ) Cytokine production of splenic cDCs from WT animals stimulated with 1 μg ml −1 LPS in the absence and presence of 60 nM non-cleavable FXII. After 48 h, cytokine concentrations were determined in culture supernatants by ELISA. ( c ) Cytokine production of splenic cDCs from CD87-deficient ( Cd87 −/− ) mice stimulated with 1 μg ml −1 LPS alone or in the absence and presence of 60 nM FXII for 48 h. ( d ) Cytokine production of splenic cDCs from CD11b-deficient ( Itgam −/− ) animals stimulated with 1 μg ml −1 LPS in the absence and presence of 60 nM FXII for 48 h. ( e ) Cytosolic cAMP formation measured in cDCs from WT or Cd87 −/− mice that were incubated with medium only (Ctrl) or stimulated with 1 μg ml −1 LPS for 10 min in the absence (Ctrl) or presence of 60 nM FXII. ( f ) Cytokine concentrations of IL-6 (left panel) and IL-23 (right panel) in the supernatants of WT cDCs stimulated with 1 μg ml −1 LPS or 60 nM FXII for 48 h in the presence of protein kinase A inhibitors (3 μM H-89 and 100 μM Rp-8-Br-cAMP). ( g ) Cytokine concentrations of IFN-γ, IL-17A, IL-6, IL-12 and IL-23 were measured in the supernatants from co-cultures of CD4 + T lymphocytes from WT (upper panel) or Cd87 −/− (lower panel) that were polyclonal activated together with cDCs from WT and Cd87 −/− in the absence or presence of 60 nM FXII. In a – g , data are given as means±s.e.m. of three independent experiments, each performed in duplicate (non-parametric Mann–Whitney U -test). * P

    Article Snippet: Astrocyte and microglia cultures were stained with anti-GFAP and anti-CD11b (1:1,000, clone EPR1344, Abcam), respectively.

    Techniques: Enzyme-linked Immunosorbent Assay, Mouse Assay, Incubation, MANN-WHITNEY

    Evidence for the involvement of FXII in human autoimmune CNS inflammation. ( a ) FXII plasma levels in individuals with clinically isolated syndrome (CIS) and MS patients (relapsing–remitting MS (RRMS), primary progressive MS (PPMS) and secondary progressive MS (SPMS)) compared with HDs. ( b ) FXII plasma levels in individuals with RRMS during relapse compared with HDs. ( c ) Correlation of FXII plasma levels with relapse-free time in individuals with RRMS. R value: −0.4226. ( d ) Histological analysis of CNS tissue from individuals with MS or from HDs. Sections were stained for FXII (red) and nucleus (4,6-diamidino-2-phenylindole (DAPI), blue). Scale bar, 100 μm. ( e ) Histological analysis of CNS tissue of individuals with MS. Sections were stained for CD11c (red), FXII (green) and nucleus (DAPI, blue). Scale bar, 100 μm. ( f – k ) Flow cytometric analysis of human PBMCs from HDs that were incubated with medium only (Ctrl) or stimulated with 60 nM FXII for 24 h. Cells were gated for CD1c + CD11c + CD11b + CD19 neg (cDC) based on indicated surface markers (shown in f ) and their expressions of ( g ) CD80, ( h ) CD86, ( i ) CD40, ( j ) MHC-II and ( k ) CD87 were determined. Representative fluorescence-activated cell sorting plots for indicated surface markers are shown. ( l ) Cytokine concentrations of IL-6 (left panel) and IL-23 (right panel) in the supernatants of human PBMCs treated with 60 nM FXII or untreated (Ctrl) for 24 h. In a , b and g – l , data are given as mean±s.e.m. (non-parametric Mann–Whitney U -test or Student's t -test). * P

    Journal: Nature Communications

    Article Title: Blood coagulation factor XII drives adaptive immunity during neuroinflammation via CD87-mediated modulation of dendritic cells

    doi: 10.1038/ncomms11626

    Figure Lengend Snippet: Evidence for the involvement of FXII in human autoimmune CNS inflammation. ( a ) FXII plasma levels in individuals with clinically isolated syndrome (CIS) and MS patients (relapsing–remitting MS (RRMS), primary progressive MS (PPMS) and secondary progressive MS (SPMS)) compared with HDs. ( b ) FXII plasma levels in individuals with RRMS during relapse compared with HDs. ( c ) Correlation of FXII plasma levels with relapse-free time in individuals with RRMS. R value: −0.4226. ( d ) Histological analysis of CNS tissue from individuals with MS or from HDs. Sections were stained for FXII (red) and nucleus (4,6-diamidino-2-phenylindole (DAPI), blue). Scale bar, 100 μm. ( e ) Histological analysis of CNS tissue of individuals with MS. Sections were stained for CD11c (red), FXII (green) and nucleus (DAPI, blue). Scale bar, 100 μm. ( f – k ) Flow cytometric analysis of human PBMCs from HDs that were incubated with medium only (Ctrl) or stimulated with 60 nM FXII for 24 h. Cells were gated for CD1c + CD11c + CD11b + CD19 neg (cDC) based on indicated surface markers (shown in f ) and their expressions of ( g ) CD80, ( h ) CD86, ( i ) CD40, ( j ) MHC-II and ( k ) CD87 were determined. Representative fluorescence-activated cell sorting plots for indicated surface markers are shown. ( l ) Cytokine concentrations of IL-6 (left panel) and IL-23 (right panel) in the supernatants of human PBMCs treated with 60 nM FXII or untreated (Ctrl) for 24 h. In a , b and g – l , data are given as mean±s.e.m. (non-parametric Mann–Whitney U -test or Student's t -test). * P

    Article Snippet: Astrocyte and microglia cultures were stained with anti-GFAP and anti-CD11b (1:1,000, clone EPR1344, Abcam), respectively.

    Techniques: Isolation, Staining, Incubation, Fluorescence, FACS, MANN-WHITNEY

    Modulation of inflammatory cells under endotoxemic conditions. (A1) CD11b-positive cells were quantified as numbers of cells per high-power field. (A2) Representative images of CD11b cells in immunostained lung specimens. (B1) Iba-1 positive cells were quantified as the number of cells per high-power field. (B2) Representative images of Iba-1 in immunostained lung samples. *, P

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: Endothelial Glycocalyx Disorders May Be Associated With Extended Inflammation During Endotoxemia in a Diabetic Mouse Model

    doi: 10.3389/fcell.2021.623582

    Figure Lengend Snippet: Modulation of inflammatory cells under endotoxemic conditions. (A1) CD11b-positive cells were quantified as numbers of cells per high-power field. (A2) Representative images of CD11b cells in immunostained lung specimens. (B1) Iba-1 positive cells were quantified as the number of cells per high-power field. (B2) Representative images of Iba-1 in immunostained lung samples. *, P

    Article Snippet: Immunohistochemistry Lung sections were incubated with primary antibodies against the neutrophil and macrophage surface marker CD11b (ab133357; Abcam, Cambridge, United Kingdom), the vascular endothelial cell marker CD31 (DIO-310; Dianova GmbH, Hamburg, Germany), and the activated macrophage surface marker Iba-1 (019-19741; Wako Pure Chemical, Osaka, Japan).

    Techniques:

    Long-term miR-143-145 deficiency results in myeloid expansion. a White blood cell (WBC), hemoglobin (HGB), and platelet (PLT) counts in peripheral blood of 80-week-old wild-type (WT; n = 28) and miR-143/145 −/− mice ( n = 23). b Micrographs of spleen sections from WT and miR-143/145 −/− mice immunostained for Mac1 (CD11b) (scale bar: 50 μm). Insets show higher magnification of selected area (scale bar: 100 μm). c Microscopic images of liver sections from WT and miR-143/145 −/− mice immunostained for CD11b (scale bar: 50 μm). Insets show higher magnification of selected area (scale bar: 100 μm). d – g Linear regression and Pearson's correlation analysis was performed on data from aged miR-143/145 −/− mice (82–101 weeks old) to compare the relationship between spleen/liver weights and WBC count ( d , e , n = 17), spleen and liver weight ( f , n = 17), and WBC count and the number of progenitors (Lin − Sca1 − c-Kit + ) ( g , n = 8)

    Journal: Nature Communications

    Article Title: miR-143/145 differentially regulate hematopoietic stem and progenitor activity through suppression of canonical TGFβ signaling

    doi: 10.1038/s41467-018-04831-3

    Figure Lengend Snippet: Long-term miR-143-145 deficiency results in myeloid expansion. a White blood cell (WBC), hemoglobin (HGB), and platelet (PLT) counts in peripheral blood of 80-week-old wild-type (WT; n = 28) and miR-143/145 −/− mice ( n = 23). b Micrographs of spleen sections from WT and miR-143/145 −/− mice immunostained for Mac1 (CD11b) (scale bar: 50 μm). Insets show higher magnification of selected area (scale bar: 100 μm). c Microscopic images of liver sections from WT and miR-143/145 −/− mice immunostained for CD11b (scale bar: 50 μm). Insets show higher magnification of selected area (scale bar: 100 μm). d – g Linear regression and Pearson's correlation analysis was performed on data from aged miR-143/145 −/− mice (82–101 weeks old) to compare the relationship between spleen/liver weights and WBC count ( d , e , n = 17), spleen and liver weight ( f , n = 17), and WBC count and the number of progenitors (Lin − Sca1 − c-Kit + ) ( g , n = 8)

    Article Snippet: In brief, tissue sections were incubated in Tris EDTA buffer at 95 °C to retrieve antigenicity, followed by incubation with the anti-CD11b primary antibody (ab133357, Abcam).

    Techniques: Mouse Assay

    Long-term miR-143-145 deficiency results in myeloid expansion. a White blood cell (WBC), hemoglobin (HGB), and platelet (PLT) counts in peripheral blood of 80-week-old wild-type (WT; n = 28) and miR-143/145 −/− mice ( n = 23). b Micrographs of spleen sections from WT and miR-143/145 −/− mice immunostained for Mac1 (CD11b) (scale bar: 50 μm). Insets show higher magnification of selected area (scale bar: 100 μm). c Microscopic images of liver sections from WT and miR-143/145 −/− mice immunostained for CD11b (scale bar: 50 μm). Insets show higher magnification of selected area (scale bar: 100 μm). d – g Linear regression and Pearson's correlation analysis was performed on data from aged miR-143/145 −/− mice (82–101 weeks old) to compare the relationship between spleen/liver weights and WBC count ( d , e , n = 17), spleen and liver weight ( f , n = 17), and WBC count and the number of progenitors (Lin − Sca1 − c-Kit + ) ( g , n = 8)

    Journal: Nature Communications

    Article Title: miR-143/145 differentially regulate hematopoietic stem and progenitor activity through suppression of canonical TGFβ signaling

    doi: 10.1038/s41467-018-04831-3

    Figure Lengend Snippet: Long-term miR-143-145 deficiency results in myeloid expansion. a White blood cell (WBC), hemoglobin (HGB), and platelet (PLT) counts in peripheral blood of 80-week-old wild-type (WT; n = 28) and miR-143/145 −/− mice ( n = 23). b Micrographs of spleen sections from WT and miR-143/145 −/− mice immunostained for Mac1 (CD11b) (scale bar: 50 μm). Insets show higher magnification of selected area (scale bar: 100 μm). c Microscopic images of liver sections from WT and miR-143/145 −/− mice immunostained for CD11b (scale bar: 50 μm). Insets show higher magnification of selected area (scale bar: 100 μm). d – g Linear regression and Pearson's correlation analysis was performed on data from aged miR-143/145 −/− mice (82–101 weeks old) to compare the relationship between spleen/liver weights and WBC count ( d , e , n = 17), spleen and liver weight ( f , n = 17), and WBC count and the number of progenitors (Lin − Sca1 − c-Kit + ) ( g , n = 8)

    Article Snippet: In brief, tissue sections were incubated in Tris EDTA buffer at 95 °C to retrieve antigenicity, followed by incubation with the anti-CD11b primary antibody (ab133357, Abcam).

    Techniques: Mouse Assay