goat anti mouse il 17 neutralizing antibody  (R&D Systems)

 
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    Name:
    Goat Anti Mouse IgM Fluorescein conjugated Antibody
    Description:
    The Goat Anti Mouse IgM Fluorescein conjugated Antibody from R D Systems is a goat polyclonal antibody to IgM This antibody reacts with mouse The Goat Anti Mouse IgM Fluorescein conjugated Antibody has been validated for the following applications Flow Cytometry
    Catalog Number:
    F0118
    Price:
    149
    Category:
    Secondary Antibodies
    Applications:
    Flow Cytometry
    Conjugate:
    Fluorescein
    Size:
    100 Tests
    Host:
    Goat
    Isotype:
    IgG
    Buy from Supplier


    Structured Review

    R&D Systems goat anti mouse il 17 neutralizing antibody
    IL-9 strengthens the survival and protumor effect of mast cells in tumor microenvironment. (A and B) Mast cells upregulated the expressions of IL-9 by Treg cells. BMMCs were injected into tumor-bearing mice with <t>IL-17</t> antibody or control antibody. Seven days later, the tumor-infiltrating Treg cells were isolated for the analysis of IL-9 by real time RT-PCR (A). Or the isolated Treg cells were cultured for 48 hours. The supernatant was used for IL-9 ELISA assay (B). (C and D) The interference of IL-9 signaling affected mast cell-mediated MDSC infiltration and mast cell-promoted tumor growth. 5×10 6 BMMCs were injected into tumor-bearing mice (n = 6) by i.v. injection. IL-9 neutralizing antibody or CD25 depleting antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. On day 12, the tumor-infiltrating lymphocytes were used to analyze Gr-1 + CD11b + MDSCs by flow cytometry (C), and the tumor growth was monitored by measuring the length (L) and width (W) of tumors. The volume (V) of the tumor was calculated by the formula V = (L×W2)/2 (D). (E) IL-9 affected the survival of mast cells in tumor microenvironment. 1×10 6 CFSE-labeled BMMCs were directly injected into tumor tissue with multiple injection sites. IL-9 neutralizing antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. The tumor tissues were surgically excised on day 7 for fluorescent analysis of frozen sections.
    The Goat Anti Mouse IgM Fluorescein conjugated Antibody from R D Systems is a goat polyclonal antibody to IgM This antibody reacts with mouse The Goat Anti Mouse IgM Fluorescein conjugated Antibody has been validated for the following applications Flow Cytometry
    https://www.bioz.com/result/goat anti mouse il 17 neutralizing antibody/product/R&D Systems
    Average 97 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    goat anti mouse il 17 neutralizing antibody - by Bioz Stars, 2021-09
    97/100 stars

    Images

    1) Product Images from "Mast Cells Mobilize Myeloid-Derived Suppressor Cells and Treg Cells in Tumor Microenvironment via IL-17 Pathway in Murine Hepatocarcinoma Model"

    Article Title: Mast Cells Mobilize Myeloid-Derived Suppressor Cells and Treg Cells in Tumor Microenvironment via IL-17 Pathway in Murine Hepatocarcinoma Model

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0008922

    IL-9 strengthens the survival and protumor effect of mast cells in tumor microenvironment. (A and B) Mast cells upregulated the expressions of IL-9 by Treg cells. BMMCs were injected into tumor-bearing mice with IL-17 antibody or control antibody. Seven days later, the tumor-infiltrating Treg cells were isolated for the analysis of IL-9 by real time RT-PCR (A). Or the isolated Treg cells were cultured for 48 hours. The supernatant was used for IL-9 ELISA assay (B). (C and D) The interference of IL-9 signaling affected mast cell-mediated MDSC infiltration and mast cell-promoted tumor growth. 5×10 6 BMMCs were injected into tumor-bearing mice (n = 6) by i.v. injection. IL-9 neutralizing antibody or CD25 depleting antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. On day 12, the tumor-infiltrating lymphocytes were used to analyze Gr-1 + CD11b + MDSCs by flow cytometry (C), and the tumor growth was monitored by measuring the length (L) and width (W) of tumors. The volume (V) of the tumor was calculated by the formula V = (L×W2)/2 (D). (E) IL-9 affected the survival of mast cells in tumor microenvironment. 1×10 6 CFSE-labeled BMMCs were directly injected into tumor tissue with multiple injection sites. IL-9 neutralizing antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. The tumor tissues were surgically excised on day 7 for fluorescent analysis of frozen sections.
    Figure Legend Snippet: IL-9 strengthens the survival and protumor effect of mast cells in tumor microenvironment. (A and B) Mast cells upregulated the expressions of IL-9 by Treg cells. BMMCs were injected into tumor-bearing mice with IL-17 antibody or control antibody. Seven days later, the tumor-infiltrating Treg cells were isolated for the analysis of IL-9 by real time RT-PCR (A). Or the isolated Treg cells were cultured for 48 hours. The supernatant was used for IL-9 ELISA assay (B). (C and D) The interference of IL-9 signaling affected mast cell-mediated MDSC infiltration and mast cell-promoted tumor growth. 5×10 6 BMMCs were injected into tumor-bearing mice (n = 6) by i.v. injection. IL-9 neutralizing antibody or CD25 depleting antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. On day 12, the tumor-infiltrating lymphocytes were used to analyze Gr-1 + CD11b + MDSCs by flow cytometry (C), and the tumor growth was monitored by measuring the length (L) and width (W) of tumors. The volume (V) of the tumor was calculated by the formula V = (L×W2)/2 (D). (E) IL-9 affected the survival of mast cells in tumor microenvironment. 1×10 6 CFSE-labeled BMMCs were directly injected into tumor tissue with multiple injection sites. IL-9 neutralizing antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. The tumor tissues were surgically excised on day 7 for fluorescent analysis of frozen sections.

    Techniques Used: Injection, Mouse Assay, Isolation, Quantitative RT-PCR, Cell Culture, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Cytometry, Labeling

    Mast cell-induced IL-17 enhances suppressor function of Treg cells via upregulating CD39 and CD73. (A) The interference of IL-17 impaired the effect of mast cells on the suppressive function of Treg cells. 5×10 6 BMMCs were injected into tumor-bearing mice by i.v. injection. IL-17 or CCL2 neutralizing antibody or Gr-1 depleting antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. On day 7, tumor-infiltrating Treg cells were isolated for suppression assay. (B and C) Mast cells had no effect on Treg cells expressing CTLA-4, IL-10 or TGF-β. BMMCs were injected into tumor-bearing mice. Seven days later, the tumor-infiltrating lymphocytes were isolated for the analysis of CTLA-4 by flow cytometry. The data showed the gated CD3 + Foxp3 + cells. (B) or IL-10 and TGF-β by real time RT-PCR (C). (D) Mast cells upregulated the expressions of CD39 and CD73 by Treg cells. BMMCs were injected into tumor-bearing mice with IL-17 antibody or control antibody. Seven days later, the tumor-infiltrating Treg cells were isolated for the analysis of CD39 and CD73 by real time RT-PCR and western blot. (E) IL-17 had no direct effect on Treg cells. IL-17 (20 ng/ml) was added to the cultured Treg cells for 12 hours. The cells were collected for the analysis of CD39 and CD73 by real time RT-PCR. F , Blockade of adenosine signaling pathway impaired mast cell-enhanced Treg cell function. BMMCs were injected into tumor-bearing mice. BM cells were used as control. Seven days later, the tumor-infiltrating Treg cells were isolated for suppression assay in the presence or absence of adenosine receptor A 2A antagonist SCH-58261 (100 ng/ml). The data shown were the representative of 2 independent experiments in which the similar results were obtained.
    Figure Legend Snippet: Mast cell-induced IL-17 enhances suppressor function of Treg cells via upregulating CD39 and CD73. (A) The interference of IL-17 impaired the effect of mast cells on the suppressive function of Treg cells. 5×10 6 BMMCs were injected into tumor-bearing mice by i.v. injection. IL-17 or CCL2 neutralizing antibody or Gr-1 depleting antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. On day 7, tumor-infiltrating Treg cells were isolated for suppression assay. (B and C) Mast cells had no effect on Treg cells expressing CTLA-4, IL-10 or TGF-β. BMMCs were injected into tumor-bearing mice. Seven days later, the tumor-infiltrating lymphocytes were isolated for the analysis of CTLA-4 by flow cytometry. The data showed the gated CD3 + Foxp3 + cells. (B) or IL-10 and TGF-β by real time RT-PCR (C). (D) Mast cells upregulated the expressions of CD39 and CD73 by Treg cells. BMMCs were injected into tumor-bearing mice with IL-17 antibody or control antibody. Seven days later, the tumor-infiltrating Treg cells were isolated for the analysis of CD39 and CD73 by real time RT-PCR and western blot. (E) IL-17 had no direct effect on Treg cells. IL-17 (20 ng/ml) was added to the cultured Treg cells for 12 hours. The cells were collected for the analysis of CD39 and CD73 by real time RT-PCR. F , Blockade of adenosine signaling pathway impaired mast cell-enhanced Treg cell function. BMMCs were injected into tumor-bearing mice. BM cells were used as control. Seven days later, the tumor-infiltrating Treg cells were isolated for suppression assay in the presence or absence of adenosine receptor A 2A antagonist SCH-58261 (100 ng/ml). The data shown were the representative of 2 independent experiments in which the similar results were obtained.

    Techniques Used: Injection, Mouse Assay, Isolation, Suppression Assay, Expressing, Flow Cytometry, Cytometry, Quantitative RT-PCR, Western Blot, Cell Culture, Cell Function Assay

    Mast cells regulate MDSCs through IL-17 pathway. (A) Blockade of IL-17 prevented mast cell-mediated MDSC infiltration to tumor. 5×10 6 BMMCs were injected into tumor-bearing mice by i.v. injection. IL-17 neutralizing antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. On day 7, the tumor-infiltrating lymphocytes were used to analyze Gr-1 + CD11b + MDSCs by flow cytometry (left). In addition, IL-17 neutralizing antibody was i.p. injected to the mice 24 h and 1 h before BMMCs injection. 2×10 6 CFSE-labeled MDSCs were injected into the mice two days later. The tumor tissues were surgically excised, and frozen sections were prepared and analyzed by fluorescence microscopy (right). (B) Blockade of IL-17 attenuated mast cell-mediated MDSC suppressive function. BMMCs were injected into tumor-bearing mice. IL-17 neutralizing antibody was i.p. injected to the mice at different time points. On day 7, tumor-infiltrating MDSCs were isolated for the suppression assay. (C) IL-17 was not expressed by H22 tumor cells, T cells or B cells. BMMCs were injected into tumor-bearing mice. Seven days later, tumor cells and TILs were isolated, respectively. The expression of IL-17 was analyzed by flow cytometry. (D and E) Mast cells upregulated the expression of IL-17 by MDSCs. Seven days after BMMCs injection, the isolated TILs were used for IL-17 expression analysis. The data showed the upregulation of IL-17 by CD11b + cells in BMMC group (D), and most of the gated IL-17 + cells expressed Gr-1 marker (E).
    Figure Legend Snippet: Mast cells regulate MDSCs through IL-17 pathway. (A) Blockade of IL-17 prevented mast cell-mediated MDSC infiltration to tumor. 5×10 6 BMMCs were injected into tumor-bearing mice by i.v. injection. IL-17 neutralizing antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. On day 7, the tumor-infiltrating lymphocytes were used to analyze Gr-1 + CD11b + MDSCs by flow cytometry (left). In addition, IL-17 neutralizing antibody was i.p. injected to the mice 24 h and 1 h before BMMCs injection. 2×10 6 CFSE-labeled MDSCs were injected into the mice two days later. The tumor tissues were surgically excised, and frozen sections were prepared and analyzed by fluorescence microscopy (right). (B) Blockade of IL-17 attenuated mast cell-mediated MDSC suppressive function. BMMCs were injected into tumor-bearing mice. IL-17 neutralizing antibody was i.p. injected to the mice at different time points. On day 7, tumor-infiltrating MDSCs were isolated for the suppression assay. (C) IL-17 was not expressed by H22 tumor cells, T cells or B cells. BMMCs were injected into tumor-bearing mice. Seven days later, tumor cells and TILs were isolated, respectively. The expression of IL-17 was analyzed by flow cytometry. (D and E) Mast cells upregulated the expression of IL-17 by MDSCs. Seven days after BMMCs injection, the isolated TILs were used for IL-17 expression analysis. The data showed the upregulation of IL-17 by CD11b + cells in BMMC group (D), and most of the gated IL-17 + cells expressed Gr-1 marker (E).

    Techniques Used: Injection, Mouse Assay, Flow Cytometry, Cytometry, Labeling, Fluorescence, Microscopy, Isolation, Suppression Assay, Expressing, Marker

    Mast cell-induced IL-17 mediates Treg cell infiltration via upregulating chemokines CCL17 and CCL22. (A) The interference of IL-17 impaired the effect of mast cells on Treg cell infiltration. 5×10 6 BMMCs were injected into tumor-bearing mice by i.v. injection. IL-17 or CCL2 neutralizing antibody or Gr-1 depleting antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. On day 7, the tumor-infiltrating lymphocytes were isolated to analyze CD3 + Foxp3 + Treg cells by flow cytometry. The results were combined from three mice. (B and C) Mast cells-induced IL-17 upregulated CCL17 and CCL22 expressions in tumor microenvironment. BMMCs were injected into tumor-bearing mice. IL-17 or Gr-1 antibody was i.p. injected to the mice at different time points. Seven days after BMMCs injection, the tumor tissues were used to analyze CCL17 and CCL22 expressions by real time RT-PCR (B) and ELISA (C). (D) The effect of CCL17 and CCL22 on Treg cell infiltration. BMMCs were injected into tumor-bearing mice. CCL17 or CCL22 neutralizing antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. On day 7, the tumor-infiltrating lymphocytes were isolated to analyze CD3 + Foxp3 + Treg cells by flow cytometry. The results were combined from three mice.
    Figure Legend Snippet: Mast cell-induced IL-17 mediates Treg cell infiltration via upregulating chemokines CCL17 and CCL22. (A) The interference of IL-17 impaired the effect of mast cells on Treg cell infiltration. 5×10 6 BMMCs were injected into tumor-bearing mice by i.v. injection. IL-17 or CCL2 neutralizing antibody or Gr-1 depleting antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. On day 7, the tumor-infiltrating lymphocytes were isolated to analyze CD3 + Foxp3 + Treg cells by flow cytometry. The results were combined from three mice. (B and C) Mast cells-induced IL-17 upregulated CCL17 and CCL22 expressions in tumor microenvironment. BMMCs were injected into tumor-bearing mice. IL-17 or Gr-1 antibody was i.p. injected to the mice at different time points. Seven days after BMMCs injection, the tumor tissues were used to analyze CCL17 and CCL22 expressions by real time RT-PCR (B) and ELISA (C). (D) The effect of CCL17 and CCL22 on Treg cell infiltration. BMMCs were injected into tumor-bearing mice. CCL17 or CCL22 neutralizing antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. On day 7, the tumor-infiltrating lymphocytes were isolated to analyze CD3 + Foxp3 + Treg cells by flow cytometry. The results were combined from three mice.

    Techniques Used: Injection, Mouse Assay, Isolation, Flow Cytometry, Cytometry, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay

    A model of the closed loop among mast cells, MDSCs and Treg cells in tumor microenvironment. Under the guidance of SCF/c-kit signaling, mast cells migrate to and are activated in tumor microenvironment; the activated mast cells release a panel of factors, leading to CCL2 production and IL-17 upregulation in MDSCs; CCL2 signaling recruits more MDSCs, leading to more IL-17 production; IL-17 strengthens tumor inflammatory microenvironment, leading to the upregulation of IL-9, IL-10, IL-13, CCL17, CCL22, CD39 and CD73; IL-10 and IL-13 induce arginase 1 expression by MDSCs; CCL17 and CCL22 attract the migration of Treg cells; CD39 and CD73 enhance suppressor function of Treg cells; IL-9 produced by Treg cells maintains the survival of mast cells; MDSCs release active MMP9, through which soluble SCF is generated, thus further facilitating the migration and activation of mast cells.
    Figure Legend Snippet: A model of the closed loop among mast cells, MDSCs and Treg cells in tumor microenvironment. Under the guidance of SCF/c-kit signaling, mast cells migrate to and are activated in tumor microenvironment; the activated mast cells release a panel of factors, leading to CCL2 production and IL-17 upregulation in MDSCs; CCL2 signaling recruits more MDSCs, leading to more IL-17 production; IL-17 strengthens tumor inflammatory microenvironment, leading to the upregulation of IL-9, IL-10, IL-13, CCL17, CCL22, CD39 and CD73; IL-10 and IL-13 induce arginase 1 expression by MDSCs; CCL17 and CCL22 attract the migration of Treg cells; CD39 and CD73 enhance suppressor function of Treg cells; IL-9 produced by Treg cells maintains the survival of mast cells; MDSCs release active MMP9, through which soluble SCF is generated, thus further facilitating the migration and activation of mast cells.

    Techniques Used: Expressing, Migration, Produced, Generated, Activation Assay

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    Blocking Assay:

    Article Title: Clusterin and Its Potential Regulatory microRNAs as a Part of Secretome for the Diagnosis of Abnormally Invasive Placenta: Accreta, Increta, and Percreta Cases
    Article Snippet: .. Western Blotting Eleven micrograms of the total protein of the plasma sample, the concentration of which was determined by the Biuret method, was (i) denatured at 65 °C for 5 min in a buffer containing 50 mM tris(hydroxymethyl)aminomethane (Sigma-Aldrich, St. Louis, MO, USA, cat. No T4661) hydrochloride (Tris-HCl) at a pH of 6.8, 1% sodium dodecyl sulfate (SDS) (VWR Life Science AMRESCO, Framingham, MA, USA, cat. No Am-O227-0.1), and 10% glycerol (AppliChem, Darmstadt, Germany, A4443), 238 mM 2-mercaptoethanol (VWR Life Science AMRESCO, Framingham, MA USA, cat. No Am-O482-0.1); (ii) separated in 10% SDS-PAGE in Tris-tricine buffer (100 mM Tris, 100 mM tricine (Sigma-Aldrich, St. Louis, MO, USA, cat. No T0377), 0.1% SDS), as recommended by H. Schägger [ ]; (iii) transferred to a PVDF membrane (0.45 µm, Immobilon, Merck Millipore Ltd., Germany, catalog No. IPVH07850) by semi-dry transfer in a Trans-blot® SD semi-dry transfer cell (BioRad, Hercules, CA, USA, cat. No 1703940) using two buffer systems (anode buffer: 40 mM 3-cyclohexylamino-1-propanesulfonic acid (CAPS) (Sigma-Aldrich, USA, cat. No SW18805), 60 mM Tris, pH = 9.6, 15% ethanol; cathode buffer: 40 mM CAPS, 60 mM Tris, pH = 9.6, 0.1% SDS) followed by membrane blocking with 1% non-fat dry milk (M7409, Sigma-Aldrich), 0.1% Tween® 20 (Sigma-Aldrich, USA, cat. No P1379), 50 mM Tris-HCl at a pH of 7.5 and 150 mM NaCl (AppliChem Panreac ITW Companies, Darmstadt, Germany, A1371); and (iv) incubated with primary mouse monoclonal antibodies to E-cadherin at a dilution of 1:400 (5F133, Santa Cruz Biotechnology, Dallas, TX, USA, cat. No sc-71007) or primary mice monoclonal antibodies to the alpha subunit of clusterin at a dilution of 1:400 (B-5, Santa Cruz Biotechnology, Dallas, TX, USA, cat. No sc-5289), followed by incubation with goat anti-mouse secondary polyclonal antibodies conjugated with horseradish peroxidase at a dilution of 1:1000 (R & D Systems, Minneapolis, MN, USA, cat. No HAF007). ..

    Mouse Assay:

    Article Title: Clusterin and Its Potential Regulatory microRNAs as a Part of Secretome for the Diagnosis of Abnormally Invasive Placenta: Accreta, Increta, and Percreta Cases
    Article Snippet: .. Western Blotting Eleven micrograms of the total protein of the plasma sample, the concentration of which was determined by the Biuret method, was (i) denatured at 65 °C for 5 min in a buffer containing 50 mM tris(hydroxymethyl)aminomethane (Sigma-Aldrich, St. Louis, MO, USA, cat. No T4661) hydrochloride (Tris-HCl) at a pH of 6.8, 1% sodium dodecyl sulfate (SDS) (VWR Life Science AMRESCO, Framingham, MA, USA, cat. No Am-O227-0.1), and 10% glycerol (AppliChem, Darmstadt, Germany, A4443), 238 mM 2-mercaptoethanol (VWR Life Science AMRESCO, Framingham, MA USA, cat. No Am-O482-0.1); (ii) separated in 10% SDS-PAGE in Tris-tricine buffer (100 mM Tris, 100 mM tricine (Sigma-Aldrich, St. Louis, MO, USA, cat. No T0377), 0.1% SDS), as recommended by H. Schägger [ ]; (iii) transferred to a PVDF membrane (0.45 µm, Immobilon, Merck Millipore Ltd., Germany, catalog No. IPVH07850) by semi-dry transfer in a Trans-blot® SD semi-dry transfer cell (BioRad, Hercules, CA, USA, cat. No 1703940) using two buffer systems (anode buffer: 40 mM 3-cyclohexylamino-1-propanesulfonic acid (CAPS) (Sigma-Aldrich, USA, cat. No SW18805), 60 mM Tris, pH = 9.6, 15% ethanol; cathode buffer: 40 mM CAPS, 60 mM Tris, pH = 9.6, 0.1% SDS) followed by membrane blocking with 1% non-fat dry milk (M7409, Sigma-Aldrich), 0.1% Tween® 20 (Sigma-Aldrich, USA, cat. No P1379), 50 mM Tris-HCl at a pH of 7.5 and 150 mM NaCl (AppliChem Panreac ITW Companies, Darmstadt, Germany, A1371); and (iv) incubated with primary mouse monoclonal antibodies to E-cadherin at a dilution of 1:400 (5F133, Santa Cruz Biotechnology, Dallas, TX, USA, cat. No sc-71007) or primary mice monoclonal antibodies to the alpha subunit of clusterin at a dilution of 1:400 (B-5, Santa Cruz Biotechnology, Dallas, TX, USA, cat. No sc-5289), followed by incubation with goat anti-mouse secondary polyclonal antibodies conjugated with horseradish peroxidase at a dilution of 1:1000 (R & D Systems, Minneapolis, MN, USA, cat. No HAF007). ..

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  • 93
    R&D Systems goat anti mouse il 17
    Tbet deficiency prevents induction of transplantation tolerance by combined co-stimulation blockade with persistent T17/Th2 skewing of alloantigen specific cytokine profile, and PMN, CD4, and <t>IL-17-producing</t> CD8 T cell infiltration. ( A ) Kaplan-Meier survival
    Goat Anti Mouse Il 17, supplied by R&D Systems, 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/goat anti mouse il 17/product/R&D Systems
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    goat anti mouse il 17 - by Bioz Stars, 2021-09
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    97
    R&D Systems goat anti mouse il 17 neutralizing antibody
    IL-9 strengthens the survival and protumor effect of mast cells in tumor microenvironment. (A and B) Mast cells upregulated the expressions of IL-9 by Treg cells. BMMCs were injected into tumor-bearing mice with <t>IL-17</t> antibody or control antibody. Seven days later, the tumor-infiltrating Treg cells were isolated for the analysis of IL-9 by real time RT-PCR (A). Or the isolated Treg cells were cultured for 48 hours. The supernatant was used for IL-9 ELISA assay (B). (C and D) The interference of IL-9 signaling affected mast cell-mediated MDSC infiltration and mast cell-promoted tumor growth. 5×10 6 BMMCs were injected into tumor-bearing mice (n = 6) by i.v. injection. IL-9 neutralizing antibody or CD25 depleting antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. On day 12, the tumor-infiltrating lymphocytes were used to analyze Gr-1 + CD11b + MDSCs by flow cytometry (C), and the tumor growth was monitored by measuring the length (L) and width (W) of tumors. The volume (V) of the tumor was calculated by the formula V = (L×W2)/2 (D). (E) IL-9 affected the survival of mast cells in tumor microenvironment. 1×10 6 CFSE-labeled BMMCs were directly injected into tumor tissue with multiple injection sites. IL-9 neutralizing antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. The tumor tissues were surgically excised on day 7 for fluorescent analysis of frozen sections.
    Goat Anti Mouse Il 17 Neutralizing Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/goat anti mouse il 17 neutralizing antibody/product/R&D Systems
    Average 97 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    goat anti mouse il 17 neutralizing antibody - by Bioz Stars, 2021-09
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    R&D Systems anti il 7 antibody
    Neutralization of <t>IL-7</t> reduces potent monocyte chemoattractants and CIA monocyte homing
    Anti Il 7 Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Tbet deficiency prevents induction of transplantation tolerance by combined co-stimulation blockade with persistent T17/Th2 skewing of alloantigen specific cytokine profile, and PMN, CD4, and IL-17-producing CD8 T cell infiltration. ( A ) Kaplan-Meier survival

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: Targeting Tim-1 to overcome resistance to transplantation tolerance mediated by CD8 T17 cells

    doi: 10.1073/pnas.0812538106

    Figure Lengend Snippet: Tbet deficiency prevents induction of transplantation tolerance by combined co-stimulation blockade with persistent T17/Th2 skewing of alloantigen specific cytokine profile, and PMN, CD4, and IL-17-producing CD8 T cell infiltration. ( A ) Kaplan-Meier survival

    Article Snippet: Frozen sections were used for immunofluorescence staining using goat anti-mouse IL-17 (R & D Systems), rat anti-Mouse CD4 and CD8 (both from BioExpress) as primary antibodies.

    Techniques: Transplantation Assay

    In vivo IL-17 neutralization inhibits rejection and facilitates allograft survival with combined co-stimulation blockade in Tbet KO recipients. ( A ) Fully mismatched cardiac allograft survival in Tbet KO recipients treated with CTLA4Ig+MR1 and anti-IL-17

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: Targeting Tim-1 to overcome resistance to transplantation tolerance mediated by CD8 T17 cells

    doi: 10.1073/pnas.0812538106

    Figure Lengend Snippet: In vivo IL-17 neutralization inhibits rejection and facilitates allograft survival with combined co-stimulation blockade in Tbet KO recipients. ( A ) Fully mismatched cardiac allograft survival in Tbet KO recipients treated with CTLA4Ig+MR1 and anti-IL-17

    Article Snippet: Frozen sections were used for immunofluorescence staining using goat anti-mouse IL-17 (R & D Systems), rat anti-Mouse CD4 and CD8 (both from BioExpress) as primary antibodies.

    Techniques: In Vivo, Neutralization

    IL-9 strengthens the survival and protumor effect of mast cells in tumor microenvironment. (A and B) Mast cells upregulated the expressions of IL-9 by Treg cells. BMMCs were injected into tumor-bearing mice with IL-17 antibody or control antibody. Seven days later, the tumor-infiltrating Treg cells were isolated for the analysis of IL-9 by real time RT-PCR (A). Or the isolated Treg cells were cultured for 48 hours. The supernatant was used for IL-9 ELISA assay (B). (C and D) The interference of IL-9 signaling affected mast cell-mediated MDSC infiltration and mast cell-promoted tumor growth. 5×10 6 BMMCs were injected into tumor-bearing mice (n = 6) by i.v. injection. IL-9 neutralizing antibody or CD25 depleting antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. On day 12, the tumor-infiltrating lymphocytes were used to analyze Gr-1 + CD11b + MDSCs by flow cytometry (C), and the tumor growth was monitored by measuring the length (L) and width (W) of tumors. The volume (V) of the tumor was calculated by the formula V = (L×W2)/2 (D). (E) IL-9 affected the survival of mast cells in tumor microenvironment. 1×10 6 CFSE-labeled BMMCs were directly injected into tumor tissue with multiple injection sites. IL-9 neutralizing antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. The tumor tissues were surgically excised on day 7 for fluorescent analysis of frozen sections.

    Journal: PLoS ONE

    Article Title: Mast Cells Mobilize Myeloid-Derived Suppressor Cells and Treg Cells in Tumor Microenvironment via IL-17 Pathway in Murine Hepatocarcinoma Model

    doi: 10.1371/journal.pone.0008922

    Figure Lengend Snippet: IL-9 strengthens the survival and protumor effect of mast cells in tumor microenvironment. (A and B) Mast cells upregulated the expressions of IL-9 by Treg cells. BMMCs were injected into tumor-bearing mice with IL-17 antibody or control antibody. Seven days later, the tumor-infiltrating Treg cells were isolated for the analysis of IL-9 by real time RT-PCR (A). Or the isolated Treg cells were cultured for 48 hours. The supernatant was used for IL-9 ELISA assay (B). (C and D) The interference of IL-9 signaling affected mast cell-mediated MDSC infiltration and mast cell-promoted tumor growth. 5×10 6 BMMCs were injected into tumor-bearing mice (n = 6) by i.v. injection. IL-9 neutralizing antibody or CD25 depleting antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. On day 12, the tumor-infiltrating lymphocytes were used to analyze Gr-1 + CD11b + MDSCs by flow cytometry (C), and the tumor growth was monitored by measuring the length (L) and width (W) of tumors. The volume (V) of the tumor was calculated by the formula V = (L×W2)/2 (D). (E) IL-9 affected the survival of mast cells in tumor microenvironment. 1×10 6 CFSE-labeled BMMCs were directly injected into tumor tissue with multiple injection sites. IL-9 neutralizing antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. The tumor tissues were surgically excised on day 7 for fluorescent analysis of frozen sections.

    Article Snippet: 12 days later, 5×106 BMMCs were injected into tumor-bearing mice via tail vein, When indicated, the mice received i.p. injection of 100 µg of goat-anti-mouse IL-17 neutralizing antibody (R & D Systems, Minneapolis, MN) or isotype control 24 h and 1 h before BMMCs injection.

    Techniques: Injection, Mouse Assay, Isolation, Quantitative RT-PCR, Cell Culture, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Cytometry, Labeling

    Mast cell-induced IL-17 enhances suppressor function of Treg cells via upregulating CD39 and CD73. (A) The interference of IL-17 impaired the effect of mast cells on the suppressive function of Treg cells. 5×10 6 BMMCs were injected into tumor-bearing mice by i.v. injection. IL-17 or CCL2 neutralizing antibody or Gr-1 depleting antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. On day 7, tumor-infiltrating Treg cells were isolated for suppression assay. (B and C) Mast cells had no effect on Treg cells expressing CTLA-4, IL-10 or TGF-β. BMMCs were injected into tumor-bearing mice. Seven days later, the tumor-infiltrating lymphocytes were isolated for the analysis of CTLA-4 by flow cytometry. The data showed the gated CD3 + Foxp3 + cells. (B) or IL-10 and TGF-β by real time RT-PCR (C). (D) Mast cells upregulated the expressions of CD39 and CD73 by Treg cells. BMMCs were injected into tumor-bearing mice with IL-17 antibody or control antibody. Seven days later, the tumor-infiltrating Treg cells were isolated for the analysis of CD39 and CD73 by real time RT-PCR and western blot. (E) IL-17 had no direct effect on Treg cells. IL-17 (20 ng/ml) was added to the cultured Treg cells for 12 hours. The cells were collected for the analysis of CD39 and CD73 by real time RT-PCR. F , Blockade of adenosine signaling pathway impaired mast cell-enhanced Treg cell function. BMMCs were injected into tumor-bearing mice. BM cells were used as control. Seven days later, the tumor-infiltrating Treg cells were isolated for suppression assay in the presence or absence of adenosine receptor A 2A antagonist SCH-58261 (100 ng/ml). The data shown were the representative of 2 independent experiments in which the similar results were obtained.

    Journal: PLoS ONE

    Article Title: Mast Cells Mobilize Myeloid-Derived Suppressor Cells and Treg Cells in Tumor Microenvironment via IL-17 Pathway in Murine Hepatocarcinoma Model

    doi: 10.1371/journal.pone.0008922

    Figure Lengend Snippet: Mast cell-induced IL-17 enhances suppressor function of Treg cells via upregulating CD39 and CD73. (A) The interference of IL-17 impaired the effect of mast cells on the suppressive function of Treg cells. 5×10 6 BMMCs were injected into tumor-bearing mice by i.v. injection. IL-17 or CCL2 neutralizing antibody or Gr-1 depleting antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. On day 7, tumor-infiltrating Treg cells were isolated for suppression assay. (B and C) Mast cells had no effect on Treg cells expressing CTLA-4, IL-10 or TGF-β. BMMCs were injected into tumor-bearing mice. Seven days later, the tumor-infiltrating lymphocytes were isolated for the analysis of CTLA-4 by flow cytometry. The data showed the gated CD3 + Foxp3 + cells. (B) or IL-10 and TGF-β by real time RT-PCR (C). (D) Mast cells upregulated the expressions of CD39 and CD73 by Treg cells. BMMCs were injected into tumor-bearing mice with IL-17 antibody or control antibody. Seven days later, the tumor-infiltrating Treg cells were isolated for the analysis of CD39 and CD73 by real time RT-PCR and western blot. (E) IL-17 had no direct effect on Treg cells. IL-17 (20 ng/ml) was added to the cultured Treg cells for 12 hours. The cells were collected for the analysis of CD39 and CD73 by real time RT-PCR. F , Blockade of adenosine signaling pathway impaired mast cell-enhanced Treg cell function. BMMCs were injected into tumor-bearing mice. BM cells were used as control. Seven days later, the tumor-infiltrating Treg cells were isolated for suppression assay in the presence or absence of adenosine receptor A 2A antagonist SCH-58261 (100 ng/ml). The data shown were the representative of 2 independent experiments in which the similar results were obtained.

    Article Snippet: 12 days later, 5×106 BMMCs were injected into tumor-bearing mice via tail vein, When indicated, the mice received i.p. injection of 100 µg of goat-anti-mouse IL-17 neutralizing antibody (R & D Systems, Minneapolis, MN) or isotype control 24 h and 1 h before BMMCs injection.

    Techniques: Injection, Mouse Assay, Isolation, Suppression Assay, Expressing, Flow Cytometry, Cytometry, Quantitative RT-PCR, Western Blot, Cell Culture, Cell Function Assay

    Mast cells regulate MDSCs through IL-17 pathway. (A) Blockade of IL-17 prevented mast cell-mediated MDSC infiltration to tumor. 5×10 6 BMMCs were injected into tumor-bearing mice by i.v. injection. IL-17 neutralizing antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. On day 7, the tumor-infiltrating lymphocytes were used to analyze Gr-1 + CD11b + MDSCs by flow cytometry (left). In addition, IL-17 neutralizing antibody was i.p. injected to the mice 24 h and 1 h before BMMCs injection. 2×10 6 CFSE-labeled MDSCs were injected into the mice two days later. The tumor tissues were surgically excised, and frozen sections were prepared and analyzed by fluorescence microscopy (right). (B) Blockade of IL-17 attenuated mast cell-mediated MDSC suppressive function. BMMCs were injected into tumor-bearing mice. IL-17 neutralizing antibody was i.p. injected to the mice at different time points. On day 7, tumor-infiltrating MDSCs were isolated for the suppression assay. (C) IL-17 was not expressed by H22 tumor cells, T cells or B cells. BMMCs were injected into tumor-bearing mice. Seven days later, tumor cells and TILs were isolated, respectively. The expression of IL-17 was analyzed by flow cytometry. (D and E) Mast cells upregulated the expression of IL-17 by MDSCs. Seven days after BMMCs injection, the isolated TILs were used for IL-17 expression analysis. The data showed the upregulation of IL-17 by CD11b + cells in BMMC group (D), and most of the gated IL-17 + cells expressed Gr-1 marker (E).

    Journal: PLoS ONE

    Article Title: Mast Cells Mobilize Myeloid-Derived Suppressor Cells and Treg Cells in Tumor Microenvironment via IL-17 Pathway in Murine Hepatocarcinoma Model

    doi: 10.1371/journal.pone.0008922

    Figure Lengend Snippet: Mast cells regulate MDSCs through IL-17 pathway. (A) Blockade of IL-17 prevented mast cell-mediated MDSC infiltration to tumor. 5×10 6 BMMCs were injected into tumor-bearing mice by i.v. injection. IL-17 neutralizing antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. On day 7, the tumor-infiltrating lymphocytes were used to analyze Gr-1 + CD11b + MDSCs by flow cytometry (left). In addition, IL-17 neutralizing antibody was i.p. injected to the mice 24 h and 1 h before BMMCs injection. 2×10 6 CFSE-labeled MDSCs were injected into the mice two days later. The tumor tissues were surgically excised, and frozen sections were prepared and analyzed by fluorescence microscopy (right). (B) Blockade of IL-17 attenuated mast cell-mediated MDSC suppressive function. BMMCs were injected into tumor-bearing mice. IL-17 neutralizing antibody was i.p. injected to the mice at different time points. On day 7, tumor-infiltrating MDSCs were isolated for the suppression assay. (C) IL-17 was not expressed by H22 tumor cells, T cells or B cells. BMMCs were injected into tumor-bearing mice. Seven days later, tumor cells and TILs were isolated, respectively. The expression of IL-17 was analyzed by flow cytometry. (D and E) Mast cells upregulated the expression of IL-17 by MDSCs. Seven days after BMMCs injection, the isolated TILs were used for IL-17 expression analysis. The data showed the upregulation of IL-17 by CD11b + cells in BMMC group (D), and most of the gated IL-17 + cells expressed Gr-1 marker (E).

    Article Snippet: 12 days later, 5×106 BMMCs were injected into tumor-bearing mice via tail vein, When indicated, the mice received i.p. injection of 100 µg of goat-anti-mouse IL-17 neutralizing antibody (R & D Systems, Minneapolis, MN) or isotype control 24 h and 1 h before BMMCs injection.

    Techniques: Injection, Mouse Assay, Flow Cytometry, Cytometry, Labeling, Fluorescence, Microscopy, Isolation, Suppression Assay, Expressing, Marker

    Mast cell-induced IL-17 mediates Treg cell infiltration via upregulating chemokines CCL17 and CCL22. (A) The interference of IL-17 impaired the effect of mast cells on Treg cell infiltration. 5×10 6 BMMCs were injected into tumor-bearing mice by i.v. injection. IL-17 or CCL2 neutralizing antibody or Gr-1 depleting antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. On day 7, the tumor-infiltrating lymphocytes were isolated to analyze CD3 + Foxp3 + Treg cells by flow cytometry. The results were combined from three mice. (B and C) Mast cells-induced IL-17 upregulated CCL17 and CCL22 expressions in tumor microenvironment. BMMCs were injected into tumor-bearing mice. IL-17 or Gr-1 antibody was i.p. injected to the mice at different time points. Seven days after BMMCs injection, the tumor tissues were used to analyze CCL17 and CCL22 expressions by real time RT-PCR (B) and ELISA (C). (D) The effect of CCL17 and CCL22 on Treg cell infiltration. BMMCs were injected into tumor-bearing mice. CCL17 or CCL22 neutralizing antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. On day 7, the tumor-infiltrating lymphocytes were isolated to analyze CD3 + Foxp3 + Treg cells by flow cytometry. The results were combined from three mice.

    Journal: PLoS ONE

    Article Title: Mast Cells Mobilize Myeloid-Derived Suppressor Cells and Treg Cells in Tumor Microenvironment via IL-17 Pathway in Murine Hepatocarcinoma Model

    doi: 10.1371/journal.pone.0008922

    Figure Lengend Snippet: Mast cell-induced IL-17 mediates Treg cell infiltration via upregulating chemokines CCL17 and CCL22. (A) The interference of IL-17 impaired the effect of mast cells on Treg cell infiltration. 5×10 6 BMMCs were injected into tumor-bearing mice by i.v. injection. IL-17 or CCL2 neutralizing antibody or Gr-1 depleting antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. On day 7, the tumor-infiltrating lymphocytes were isolated to analyze CD3 + Foxp3 + Treg cells by flow cytometry. The results were combined from three mice. (B and C) Mast cells-induced IL-17 upregulated CCL17 and CCL22 expressions in tumor microenvironment. BMMCs were injected into tumor-bearing mice. IL-17 or Gr-1 antibody was i.p. injected to the mice at different time points. Seven days after BMMCs injection, the tumor tissues were used to analyze CCL17 and CCL22 expressions by real time RT-PCR (B) and ELISA (C). (D) The effect of CCL17 and CCL22 on Treg cell infiltration. BMMCs were injected into tumor-bearing mice. CCL17 or CCL22 neutralizing antibody was i.p. injected to the mice 1 h, 2 days and 5 days after BMMCs injection. On day 7, the tumor-infiltrating lymphocytes were isolated to analyze CD3 + Foxp3 + Treg cells by flow cytometry. The results were combined from three mice.

    Article Snippet: 12 days later, 5×106 BMMCs were injected into tumor-bearing mice via tail vein, When indicated, the mice received i.p. injection of 100 µg of goat-anti-mouse IL-17 neutralizing antibody (R & D Systems, Minneapolis, MN) or isotype control 24 h and 1 h before BMMCs injection.

    Techniques: Injection, Mouse Assay, Isolation, Flow Cytometry, Cytometry, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay

    A model of the closed loop among mast cells, MDSCs and Treg cells in tumor microenvironment. Under the guidance of SCF/c-kit signaling, mast cells migrate to and are activated in tumor microenvironment; the activated mast cells release a panel of factors, leading to CCL2 production and IL-17 upregulation in MDSCs; CCL2 signaling recruits more MDSCs, leading to more IL-17 production; IL-17 strengthens tumor inflammatory microenvironment, leading to the upregulation of IL-9, IL-10, IL-13, CCL17, CCL22, CD39 and CD73; IL-10 and IL-13 induce arginase 1 expression by MDSCs; CCL17 and CCL22 attract the migration of Treg cells; CD39 and CD73 enhance suppressor function of Treg cells; IL-9 produced by Treg cells maintains the survival of mast cells; MDSCs release active MMP9, through which soluble SCF is generated, thus further facilitating the migration and activation of mast cells.

    Journal: PLoS ONE

    Article Title: Mast Cells Mobilize Myeloid-Derived Suppressor Cells and Treg Cells in Tumor Microenvironment via IL-17 Pathway in Murine Hepatocarcinoma Model

    doi: 10.1371/journal.pone.0008922

    Figure Lengend Snippet: A model of the closed loop among mast cells, MDSCs and Treg cells in tumor microenvironment. Under the guidance of SCF/c-kit signaling, mast cells migrate to and are activated in tumor microenvironment; the activated mast cells release a panel of factors, leading to CCL2 production and IL-17 upregulation in MDSCs; CCL2 signaling recruits more MDSCs, leading to more IL-17 production; IL-17 strengthens tumor inflammatory microenvironment, leading to the upregulation of IL-9, IL-10, IL-13, CCL17, CCL22, CD39 and CD73; IL-10 and IL-13 induce arginase 1 expression by MDSCs; CCL17 and CCL22 attract the migration of Treg cells; CD39 and CD73 enhance suppressor function of Treg cells; IL-9 produced by Treg cells maintains the survival of mast cells; MDSCs release active MMP9, through which soluble SCF is generated, thus further facilitating the migration and activation of mast cells.

    Article Snippet: 12 days later, 5×106 BMMCs were injected into tumor-bearing mice via tail vein, When indicated, the mice received i.p. injection of 100 µg of goat-anti-mouse IL-17 neutralizing antibody (R & D Systems, Minneapolis, MN) or isotype control 24 h and 1 h before BMMCs injection.

    Techniques: Expressing, Migration, Produced, Generated, Activation Assay

    Neutralization of IL-7 reduces potent monocyte chemoattractants and CIA monocyte homing

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: The novel role of IL-7 ligation to IL-7R in myeloid cells of rheumatoid arthritis and collagen induced arthritis

    doi: 10.4049/jimmunol.1201675

    Figure Lengend Snippet: Neutralization of IL-7 reduces potent monocyte chemoattractants and CIA monocyte homing

    Article Snippet: To show that RA synovial fluid mediated monocyte chemotaxis is in part due to IL-7 function, 12 synovial fluids were diluted (1:20) and neutralized with anti-IL-7 antibody (10μg/ml; R & D Systems) or control IgG.

    Techniques: Neutralization

    Spleen TH-1 cells, TH-17 cells and TH-17 promoting cytokines as well as joint CD3 immunostaining were unaffected by anti-IL-7 antibody treatment and schematic representation of the mechanism that contributes to IL-7 mediated pathogenesis in RA and CIA

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: The novel role of IL-7 ligation to IL-7R in myeloid cells of rheumatoid arthritis and collagen induced arthritis

    doi: 10.4049/jimmunol.1201675

    Figure Lengend Snippet: Spleen TH-1 cells, TH-17 cells and TH-17 promoting cytokines as well as joint CD3 immunostaining were unaffected by anti-IL-7 antibody treatment and schematic representation of the mechanism that contributes to IL-7 mediated pathogenesis in RA and CIA

    Article Snippet: To show that RA synovial fluid mediated monocyte chemotaxis is in part due to IL-7 function, 12 synovial fluids were diluted (1:20) and neutralized with anti-IL-7 antibody (10μg/ml; R & D Systems) or control IgG.

    Techniques: Immunostaining

    IL-7 induces monocyte migration through ligation to IL-7R and activation of AKT1/PI3K and ERK pathways

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: The novel role of IL-7 ligation to IL-7R in myeloid cells of rheumatoid arthritis and collagen induced arthritis

    doi: 10.4049/jimmunol.1201675

    Figure Lengend Snippet: IL-7 induces monocyte migration through ligation to IL-7R and activation of AKT1/PI3K and ERK pathways

    Article Snippet: To show that RA synovial fluid mediated monocyte chemotaxis is in part due to IL-7 function, 12 synovial fluids were diluted (1:20) and neutralized with anti-IL-7 antibody (10μg/ml; R & D Systems) or control IgG.

    Techniques: Migration, Ligation, Activation Assay

    Inhibition of AKT and ERK cascades suppresses IL-7 mediated monocyte homing, and like in RA IL-7R is expressed in CIA ST lining and sublining macrophages and sublining endothelial cells

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: The novel role of IL-7 ligation to IL-7R in myeloid cells of rheumatoid arthritis and collagen induced arthritis

    doi: 10.4049/jimmunol.1201675

    Figure Lengend Snippet: Inhibition of AKT and ERK cascades suppresses IL-7 mediated monocyte homing, and like in RA IL-7R is expressed in CIA ST lining and sublining macrophages and sublining endothelial cells

    Article Snippet: To show that RA synovial fluid mediated monocyte chemotaxis is in part due to IL-7 function, 12 synovial fluids were diluted (1:20) and neutralized with anti-IL-7 antibody (10μg/ml; R & D Systems) or control IgG.

    Techniques: Inhibition

    Therapeutic treatment of anti-IL-7 antibody ameliorates CIA pathology and bone erosion

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: The novel role of IL-7 ligation to IL-7R in myeloid cells of rheumatoid arthritis and collagen induced arthritis

    doi: 10.4049/jimmunol.1201675

    Figure Lengend Snippet: Therapeutic treatment of anti-IL-7 antibody ameliorates CIA pathology and bone erosion

    Article Snippet: To show that RA synovial fluid mediated monocyte chemotaxis is in part due to IL-7 function, 12 synovial fluids were diluted (1:20) and neutralized with anti-IL-7 antibody (10μg/ml; R & D Systems) or control IgG.

    Techniques:

    MIP-2 and joint vascularization is reduced in CIA mice treated with anti-IL-7 antibody compared to the control group

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: The novel role of IL-7 ligation to IL-7R in myeloid cells of rheumatoid arthritis and collagen induced arthritis

    doi: 10.4049/jimmunol.1201675

    Figure Lengend Snippet: MIP-2 and joint vascularization is reduced in CIA mice treated with anti-IL-7 antibody compared to the control group

    Article Snippet: To show that RA synovial fluid mediated monocyte chemotaxis is in part due to IL-7 function, 12 synovial fluids were diluted (1:20) and neutralized with anti-IL-7 antibody (10μg/ml; R & D Systems) or control IgG.

    Techniques: Mouse Assay

    IL-7 and IL-7R expression correlates with DAS28 and TNF-α levels in RA monocytes and ligation of RA synovial fluid IL-7 to myeloid IL-7R promotes chemotaxis

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: The novel role of IL-7 ligation to IL-7R in myeloid cells of rheumatoid arthritis and collagen induced arthritis

    doi: 10.4049/jimmunol.1201675

    Figure Lengend Snippet: IL-7 and IL-7R expression correlates with DAS28 and TNF-α levels in RA monocytes and ligation of RA synovial fluid IL-7 to myeloid IL-7R promotes chemotaxis

    Article Snippet: To show that RA synovial fluid mediated monocyte chemotaxis is in part due to IL-7 function, 12 synovial fluids were diluted (1:20) and neutralized with anti-IL-7 antibody (10μg/ml; R & D Systems) or control IgG.

    Techniques: Expressing, Ligation, Chemotaxis Assay

    Assessment of IL-7 expression in human LN LECs. (A) Fetal LN sections were stained with fluorescently labeled antibodies against LyveI, MadCAM-1, and CD3. (B) Adult LN sections were stained with antibodies against LyveI, VCAM-1, MadCAM-1, and Pdpn. LyveI + Pdpn + LECs (blue in left panel and green in right panel) are indicated in the subcapsular sinus (arrows) and LN medulla (*). (C) CD31 + Pdpn + LECs, CD31 − Pdpn + FRCs, and CD31 + Pdpn − BECs from human fetal mesenteric LNs were sorted by flow cytometry. IL-7 expression levels were determined by quantitative RT-PCR. Values indicate mean ± SEM from triplicates, representative results from 1 of 2 independent sorting experiments. (D) Human LN LECs were cultivated and analyzed for IL-7 mRNA expression by quantitative RT-PCR. Cell culture supernatants were collected after 48 hours and analyzed for IL-7 protein by ELISA (right graph). Measurements were carried out in triplicates (mean ± SEM). (E) MACS-isolated human naive CD4 + T cells (2 × 10 5 ) were cocultured with human LECs, HUVECs, or supernatant from human LEC cultures in the presence and absence of neutralizing anti–IL-7 antibody. After 48 hours, T-cell survival was analyzed by flow cytometry and is displayed as difference (Δ) to medium control. Values indicate mean ± SEM from triplicates, representative results from 1 of 2 independent experiments; * P

    Journal: Blood

    Article Title: IL-7-producing stromal cells are critical for lymph node remodeling

    doi: 10.1182/blood-2012-03-416859

    Figure Lengend Snippet: Assessment of IL-7 expression in human LN LECs. (A) Fetal LN sections were stained with fluorescently labeled antibodies against LyveI, MadCAM-1, and CD3. (B) Adult LN sections were stained with antibodies against LyveI, VCAM-1, MadCAM-1, and Pdpn. LyveI + Pdpn + LECs (blue in left panel and green in right panel) are indicated in the subcapsular sinus (arrows) and LN medulla (*). (C) CD31 + Pdpn + LECs, CD31 − Pdpn + FRCs, and CD31 + Pdpn − BECs from human fetal mesenteric LNs were sorted by flow cytometry. IL-7 expression levels were determined by quantitative RT-PCR. Values indicate mean ± SEM from triplicates, representative results from 1 of 2 independent sorting experiments. (D) Human LN LECs were cultivated and analyzed for IL-7 mRNA expression by quantitative RT-PCR. Cell culture supernatants were collected after 48 hours and analyzed for IL-7 protein by ELISA (right graph). Measurements were carried out in triplicates (mean ± SEM). (E) MACS-isolated human naive CD4 + T cells (2 × 10 5 ) were cocultured with human LECs, HUVECs, or supernatant from human LEC cultures in the presence and absence of neutralizing anti–IL-7 antibody. After 48 hours, T-cell survival was analyzed by flow cytometry and is displayed as difference (Δ) to medium control. Values indicate mean ± SEM from triplicates, representative results from 1 of 2 independent experiments; * P

    Article Snippet: IL-7 was neutralized using a commercially available anti–IL-7 antibody (R & D Systems).

    Techniques: Expressing, Staining, Labeling, Flow Cytometry, Cytometry, Quantitative RT-PCR, Cell Culture, Enzyme-linked Immunosorbent Assay, Magnetic Cell Separation, Isolation