anti human tnf  (Thermo Fisher)


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  • 97
    Name:
    F ab 2 Goat anti Human IgM IgG Functional Grade Secondary Antibody
    Description:
    F ab 2 Goat anti Human IgM IgG Functional Grade Secondary Antibody for Flow FN
    Catalog Number:
    16-5099-85
    Price:
    None
    Category:
    Antibodies Secondary Detection Reagents
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    Structured Review

    Thermo Fisher anti human tnf
    <t>TNF</t> and <t>IFN-β</t> are required for potent restriction of MV infection in primary human fibroblasts. (A) Primary human skin fibroblasts CCD-922Sk were mock-infected or infected with MV. X-gal staining was performed to visualize blue MV foci 48 h after infection. (B) CCD-922Sk fibroblasts were infected with MV in the absence or presence of TNF or IFN-β alone or TNF plus IFN-β. MV yields were determined by the standard plaque assay using BGMK cells at 48 h after infection. (C) CCD-922Sk fibroblasts were infected with the control MV (constructed with the same vector but no human TNF gene) or the recombinant MV expressing human TNF (MV-hTNF) in the absence or presence of IFN-β. The viral yields of both control MV and MV-hTNF were determined by the standard plaque assay using RK-13 cells at 48 h after infection. (D) CCD-922Sk fibroblasts were infected with EMCV in the absence or presence of IFN-β or TNF. EMCV quantities were titrated by the standard plaque assay using BHK cells at 48 h after infection. Data in (B), (C) and (D) represent mean +/− SD.
    F ab 2 Goat anti Human IgM IgG Functional Grade Secondary Antibody for Flow FN
    https://www.bioz.com/result/anti human tnf/product/Thermo Fisher
    Average 97 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti human tnf - by Bioz Stars, 2021-06
    97/100 stars

    Images

    1) Product Images from "RIG-I Mediates the Co-Induction of Tumor Necrosis Factor and Type I Interferon Elicited by Myxoma Virus in Primary Human Macrophages"

    Article Title: RIG-I Mediates the Co-Induction of Tumor Necrosis Factor and Type I Interferon Elicited by Myxoma Virus in Primary Human Macrophages

    Journal: PLoS Pathogens

    doi: 10.1371/journal.ppat.1000099

    TNF and IFN-β are required for potent restriction of MV infection in primary human fibroblasts. (A) Primary human skin fibroblasts CCD-922Sk were mock-infected or infected with MV. X-gal staining was performed to visualize blue MV foci 48 h after infection. (B) CCD-922Sk fibroblasts were infected with MV in the absence or presence of TNF or IFN-β alone or TNF plus IFN-β. MV yields were determined by the standard plaque assay using BGMK cells at 48 h after infection. (C) CCD-922Sk fibroblasts were infected with the control MV (constructed with the same vector but no human TNF gene) or the recombinant MV expressing human TNF (MV-hTNF) in the absence or presence of IFN-β. The viral yields of both control MV and MV-hTNF were determined by the standard plaque assay using RK-13 cells at 48 h after infection. (D) CCD-922Sk fibroblasts were infected with EMCV in the absence or presence of IFN-β or TNF. EMCV quantities were titrated by the standard plaque assay using BHK cells at 48 h after infection. Data in (B), (C) and (D) represent mean +/− SD.
    Figure Legend Snippet: TNF and IFN-β are required for potent restriction of MV infection in primary human fibroblasts. (A) Primary human skin fibroblasts CCD-922Sk were mock-infected or infected with MV. X-gal staining was performed to visualize blue MV foci 48 h after infection. (B) CCD-922Sk fibroblasts were infected with MV in the absence or presence of TNF or IFN-β alone or TNF plus IFN-β. MV yields were determined by the standard plaque assay using BGMK cells at 48 h after infection. (C) CCD-922Sk fibroblasts were infected with the control MV (constructed with the same vector but no human TNF gene) or the recombinant MV expressing human TNF (MV-hTNF) in the absence or presence of IFN-β. The viral yields of both control MV and MV-hTNF were determined by the standard plaque assay using RK-13 cells at 48 h after infection. (D) CCD-922Sk fibroblasts were infected with EMCV in the absence or presence of IFN-β or TNF. EMCV quantities were titrated by the standard plaque assay using BHK cells at 48 h after infection. Data in (B), (C) and (D) represent mean +/− SD.

    Techniques Used: Infection, Staining, Plaque Assay, Construct, Plasmid Preparation, Recombinant, Expressing

    MV-elicited production of TNF and IFN-β is mediated by RIG-I in primary human macrophages. (A) pHMs were transfected with control siRNA or siRNAs targeting cytoplasmic RNA sensors RIG-I (top panel) or MDA5 (middle panel). The cells were analyzed 48 h later by RT-PCR for the indicated mRNA levels. GAPDH was used as control. (B, C) RIG-I is critically required for MV-elicited production of both TNF (B) and IFN-β (C) in pHMs. pHMs or various siRNA pHMs were mock-infected or infected with MV and the accumulation of TNF and IFN-β in the culture supernatants was assessed by ELISA 24 h post-infection. (D) RIG-I mediates cellular restriction to MV infection in pHMs. pHMs or control siRNA or RIG-I siRNA pHMs as indicated were infected with MV. MV yields were determined by the standard plaque assay using BGMK cells at 48 h after infection. Data in (B), (C) and (D) represent mean +/− SD.
    Figure Legend Snippet: MV-elicited production of TNF and IFN-β is mediated by RIG-I in primary human macrophages. (A) pHMs were transfected with control siRNA or siRNAs targeting cytoplasmic RNA sensors RIG-I (top panel) or MDA5 (middle panel). The cells were analyzed 48 h later by RT-PCR for the indicated mRNA levels. GAPDH was used as control. (B, C) RIG-I is critically required for MV-elicited production of both TNF (B) and IFN-β (C) in pHMs. pHMs or various siRNA pHMs were mock-infected or infected with MV and the accumulation of TNF and IFN-β in the culture supernatants was assessed by ELISA 24 h post-infection. (D) RIG-I mediates cellular restriction to MV infection in pHMs. pHMs or control siRNA or RIG-I siRNA pHMs as indicated were infected with MV. MV yields were determined by the standard plaque assay using BGMK cells at 48 h after infection. Data in (B), (C) and (D) represent mean +/− SD.

    Techniques Used: Transfection, Reverse Transcription Polymerase Chain Reaction, Infection, Enzyme-linked Immunosorbent Assay, Plaque Assay

    Primary human macrophages produce TNF and IFN-β in response to MV infection. (A, B) Primary human macrophages (pHMs), CCD-922Sk fibroblasts and primary human lymphocytes were mock-infected or infected with MV. TNF (A) and IFN-β (B) accumulation in the culture supernatants was assessed by ELISA 24 h post-infection. (C) pHMs were mock-infected or infected with MV in the absence or presence of TNF neutralizing antibody (Ab) or IFN-α/β neutralizing Ab alone or TNF Ab plus IFN-α/β Ab as specified. MV β-gal activity was determined by measuring absorbance at 420 nm and normalized to the total cellular protein levels at 48 h after infection. (D) pHMs were infected with MV or UV-inactivated MV for various times (below lanes) and total RNA was analyzed by RT-PCR for induction of TNF and IFN-β mRNA. GAPDH was used as control. Data in (A), (B) and (C) represent mean +/− SD.
    Figure Legend Snippet: Primary human macrophages produce TNF and IFN-β in response to MV infection. (A, B) Primary human macrophages (pHMs), CCD-922Sk fibroblasts and primary human lymphocytes were mock-infected or infected with MV. TNF (A) and IFN-β (B) accumulation in the culture supernatants was assessed by ELISA 24 h post-infection. (C) pHMs were mock-infected or infected with MV in the absence or presence of TNF neutralizing antibody (Ab) or IFN-α/β neutralizing Ab alone or TNF Ab plus IFN-α/β Ab as specified. MV β-gal activity was determined by measuring absorbance at 420 nm and normalized to the total cellular protein levels at 48 h after infection. (D) pHMs were infected with MV or UV-inactivated MV for various times (below lanes) and total RNA was analyzed by RT-PCR for induction of TNF and IFN-β mRNA. GAPDH was used as control. Data in (A), (B) and (C) represent mean +/− SD.

    Techniques Used: Infection, Enzyme-linked Immunosorbent Assay, Activity Assay, Reverse Transcription Polymerase Chain Reaction

    IRF7 is crucial for sustaining MV-elicited TNF induction in primary human macrophages. (A) Control siRNA pHMs or IRF7 siRNA pHMs were infected with MV for various times (below lanes) and the whole cell lysates were analyzed for MV-induced expression of IRF7 protein. β-actin was used as control. (B) pHMs or various siRNA pHMs were mock-infected or infected with MV. TNF protein in the culture supernatants was assessed by ELISA 24 h post-infection. (C) IRF7 expression and TNF production kinetics. Control siRNA pHMs or IRF7 siRNA pHMs were infected with MV for various times as indicated and TNF protein in the culture supernatants was assessed by ELISA. (D) IRF7 is required for sustaining TNF gene transcription activated by MV infection. Control siRNA pHMs or IRF7 siRNA pHMs were infected with MV for various times (below lanes) and the cells were analyzed by RT-PCR for the indicated TNF mRNA levels. GAPDH was used as control. Data in (B) and (C) represent mean +/− SD.
    Figure Legend Snippet: IRF7 is crucial for sustaining MV-elicited TNF induction in primary human macrophages. (A) Control siRNA pHMs or IRF7 siRNA pHMs were infected with MV for various times (below lanes) and the whole cell lysates were analyzed for MV-induced expression of IRF7 protein. β-actin was used as control. (B) pHMs or various siRNA pHMs were mock-infected or infected with MV. TNF protein in the culture supernatants was assessed by ELISA 24 h post-infection. (C) IRF7 expression and TNF production kinetics. Control siRNA pHMs or IRF7 siRNA pHMs were infected with MV for various times as indicated and TNF protein in the culture supernatants was assessed by ELISA. (D) IRF7 is required for sustaining TNF gene transcription activated by MV infection. Control siRNA pHMs or IRF7 siRNA pHMs were infected with MV for various times (below lanes) and the cells were analyzed by RT-PCR for the indicated TNF mRNA levels. GAPDH was used as control. Data in (B) and (C) represent mean +/− SD.

    Techniques Used: Infection, Expressing, Enzyme-linked Immunosorbent Assay, Reverse Transcription Polymerase Chain Reaction

    IRF3 is critical for triggering MV-elicited TNF induction in primary human macrophages. (A) pHMs were transfected with control siRNA or MAVS siRNA. The cells were analyzed 48 h later by RT-PCR for the indicated mRNA levels. GAPDH was used as the control. (B) Control siRNA pHMs or RIG-I siRNA or MAVS siRNA pHMs as indicated were infected with MV for various times (below lanes) and the nuclear extracts were probed for nuclear IRF3 (nuc-IRF3). Nuclear USF2 (nuc-USF2) was used as nuclear protein loading control. (C) Control siRNA pHMs or RIG-I siRNA or MAVS siRNA pHMs as indicated were infected with MV for 0 h or 10 h and were immunofluorescence-stained for IRF3 (red). Nuclear DNA was counterstained with DAPI (blue). Bars are 10 µm. (D) pHMs were transfected with control siRNA or IRF3 siRNA as indicated and were analyzed 72 h later by immunoblotting for IRF3 protein levels. β-actin was used as control. (E) pHMs or various siRNA pHMs as indicated were infected with MV for 24 h and TNF protein in the culture supernatants was assessed by ELISA. Data represent mean +/− SD. (F) Control siRNA pHMs or IRF3 siRNA pHMs were infected with MV for various times (below lanes) and the cells were analyzed by RT-PCR for the indicated TNF mRNA levels. GAPDH was used as control.
    Figure Legend Snippet: IRF3 is critical for triggering MV-elicited TNF induction in primary human macrophages. (A) pHMs were transfected with control siRNA or MAVS siRNA. The cells were analyzed 48 h later by RT-PCR for the indicated mRNA levels. GAPDH was used as the control. (B) Control siRNA pHMs or RIG-I siRNA or MAVS siRNA pHMs as indicated were infected with MV for various times (below lanes) and the nuclear extracts were probed for nuclear IRF3 (nuc-IRF3). Nuclear USF2 (nuc-USF2) was used as nuclear protein loading control. (C) Control siRNA pHMs or RIG-I siRNA or MAVS siRNA pHMs as indicated were infected with MV for 0 h or 10 h and were immunofluorescence-stained for IRF3 (red). Nuclear DNA was counterstained with DAPI (blue). Bars are 10 µm. (D) pHMs were transfected with control siRNA or IRF3 siRNA as indicated and were analyzed 72 h later by immunoblotting for IRF3 protein levels. β-actin was used as control. (E) pHMs or various siRNA pHMs as indicated were infected with MV for 24 h and TNF protein in the culture supernatants was assessed by ELISA. Data represent mean +/− SD. (F) Control siRNA pHMs or IRF3 siRNA pHMs were infected with MV for various times (below lanes) and the cells were analyzed by RT-PCR for the indicated TNF mRNA levels. GAPDH was used as control.

    Techniques Used: Transfection, Reverse Transcription Polymerase Chain Reaction, Infection, Immunofluorescence, Staining, Enzyme-linked Immunosorbent Assay

    Related Articles

    Purification:

    Article Title: The Selective Phosphoinoside-3-Kinase p110δ Inhibitor IPI-3063 Potently Suppresses B Cell Survival, Proliferation, and Differentiation
    Article Snippet: B-cell purity was increased from 4% to > 70% as measured by FACS analysis (FACSCalibur and CellQuest software; BD Biosciences) using anti-CD19 PE conjugated antibody (eBioscience). .. Purified B cells were seeded at a final concentration of 0.1 × 106 cells/mL and cultured with 2 µg/mL human CD40L (eBioscience) + 5 µg/mL anti-human IgM/IgG (eBioscience) + 100 µg/mL hIL-2 (R & D Systems) + 100 µg/mL hIL-21 (R & D Systems). .. All B cells were cultured in RPMI 1640 supplemented with 10% (vol/vol) heat-inactivated FCS, 5 mM Hepes, 2 mM l -glutamine, 100 U/mL penicillin, 100 µg/mL streptomycin, 50 µM 2-mercaptoethanol.

    Concentration Assay:

    Article Title: The Selective Phosphoinoside-3-Kinase p110δ Inhibitor IPI-3063 Potently Suppresses B Cell Survival, Proliferation, and Differentiation
    Article Snippet: B-cell purity was increased from 4% to > 70% as measured by FACS analysis (FACSCalibur and CellQuest software; BD Biosciences) using anti-CD19 PE conjugated antibody (eBioscience). .. Purified B cells were seeded at a final concentration of 0.1 × 106 cells/mL and cultured with 2 µg/mL human CD40L (eBioscience) + 5 µg/mL anti-human IgM/IgG (eBioscience) + 100 µg/mL hIL-2 (R & D Systems) + 100 µg/mL hIL-21 (R & D Systems). .. All B cells were cultured in RPMI 1640 supplemented with 10% (vol/vol) heat-inactivated FCS, 5 mM Hepes, 2 mM l -glutamine, 100 U/mL penicillin, 100 µg/mL streptomycin, 50 µM 2-mercaptoethanol.

    Cell Culture:

    Article Title: The Selective Phosphoinoside-3-Kinase p110δ Inhibitor IPI-3063 Potently Suppresses B Cell Survival, Proliferation, and Differentiation
    Article Snippet: B-cell purity was increased from 4% to > 70% as measured by FACS analysis (FACSCalibur and CellQuest software; BD Biosciences) using anti-CD19 PE conjugated antibody (eBioscience). .. Purified B cells were seeded at a final concentration of 0.1 × 106 cells/mL and cultured with 2 µg/mL human CD40L (eBioscience) + 5 µg/mL anti-human IgM/IgG (eBioscience) + 100 µg/mL hIL-2 (R & D Systems) + 100 µg/mL hIL-21 (R & D Systems). .. All B cells were cultured in RPMI 1640 supplemented with 10% (vol/vol) heat-inactivated FCS, 5 mM Hepes, 2 mM l -glutamine, 100 U/mL penicillin, 100 µg/mL streptomycin, 50 µM 2-mercaptoethanol.

    Immunocytochemistry:

    Article Title: The Human Adenocarcinoma-associated Gene, AGR2, Induces Expression of Amphiregulin through Hippo Pathway Co-activator YAP1 Activation *
    Article Snippet: Primary antibodies used included: β-actin (A2066, Sigma-Aldrich Inc.), AKT (9272, Cell Signaling Technology, Danvers, MA), pAKT (4058, Cell Signaling), Erk1/2 (9102, Cell Signaling), pErk1/2 (9106, Cell Signaling), pYAP (4911, Cell Signaling), pEGFR (2236, Cell Signaling), YAP (sc-15407, Santa Cruz Biotechnology, Santa Cruz, CA), EGFR ( , Transduction Laboratories, Lexington, KY), and a neutralization antibody for AREG (AF262, R & D Systems, Minneapolis, MN). .. Anti-human AREG antibody used for immunocytochemistry was obtained from ThermoScientific and was generated against amino acids 8–26 of secreted AREG (RB-257P, Thermo Scientific). .. The characterization of the anti-AREG antibody in immunocytochemistry can be found in the following references ( – ).

    Generated:

    Article Title: The Human Adenocarcinoma-associated Gene, AGR2, Induces Expression of Amphiregulin through Hippo Pathway Co-activator YAP1 Activation *
    Article Snippet: Primary antibodies used included: β-actin (A2066, Sigma-Aldrich Inc.), AKT (9272, Cell Signaling Technology, Danvers, MA), pAKT (4058, Cell Signaling), Erk1/2 (9102, Cell Signaling), pErk1/2 (9106, Cell Signaling), pYAP (4911, Cell Signaling), pEGFR (2236, Cell Signaling), YAP (sc-15407, Santa Cruz Biotechnology, Santa Cruz, CA), EGFR ( , Transduction Laboratories, Lexington, KY), and a neutralization antibody for AREG (AF262, R & D Systems, Minneapolis, MN). .. Anti-human AREG antibody used for immunocytochemistry was obtained from ThermoScientific and was generated against amino acids 8–26 of secreted AREG (RB-257P, Thermo Scientific). .. The characterization of the anti-AREG antibody in immunocytochemistry can be found in the following references ( – ).

    Labeling:

    Article Title: Multidimensional analysis of the frequencies and rates of cytokine secretion from single cells by quantitative microengraving
    Article Snippet: The array of wells was then rinsed gently with media containing a trace amount of human serum (1:40,000) (to label the locations of all microwells with human Ig) and immediately applied onto a glass slide pre-coated with capture antibodies for 2 h. A portion of the cells used in these experiments were also stimulated in bulk, and then collected for mRNA quantification by real-time PCR at intervals matched to the microengraving. .. Alexa Fluor 488 ( , Invitrogen) labeled goat anti-human IL-6 (AF-206-NA, R & D) and Alexa Fluor 700 ( , Invitrogen) labeled goat anti-human IgG (109-175-098, Jackson Immune Research) were used for detection. ..

    Transduction:

    Article Title: RIG-I Mediates the Co-Induction of Tumor Necrosis Factor and Type I Interferon Elicited by Myxoma Virus in Primary Human Macrophages
    Article Snippet: Two cytokines were either added alone or together to the media when the infection with MV or EMCV was started and maintained throughout the entire treatment period. .. The primary antibodies were obtained from the following suppliers: anti-IRF3, anti-IRF7, anti-NF-κB p65 and anti-USF2 antibodies, Santa Cruz Biotechnology; anti-human TNF and anti-human IFN-α/β antibodies, Biosource International; anti-β-actin antibody, Sigma; anti-STAT1 antibody, Transduction Laboratories. ..

    Functional Assay:

    Article Title: Intracellular Networks of the PI3K/AKT and MAPK Pathways for Regulating Toxoplasma gondii-Induced IL-23 and IL-12 Production in Human THP-1 Cells
    Article Snippet: Antibody neutralization assay THP-1 cells (1.0 × 106 cells/mL) were added to a 48-well cell culture plate and pre-treated with 1–10 μg/mL TLR2 and TLR4 monoclonal antibodies, or IgG isotype control for 1 h at 37°C in 5% CO2 . .. Antibodies and isotype controls used were functional grade anti-human TLR2, TLR4 and IgG isotype control antibodies from eBioscience. .. Following the 1 h incubation, T . gondii tachyzoites infected into THP-1 cells in the continuing presence of neutralizing antibodies and the cells were further incubated for 18 h in the same conditions.

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  • 97
    Thermo Fisher anti human tnf
    <t>TNF</t> and <t>IFN-β</t> are required for potent restriction of MV infection in primary human fibroblasts. (A) Primary human skin fibroblasts CCD-922Sk were mock-infected or infected with MV. X-gal staining was performed to visualize blue MV foci 48 h after infection. (B) CCD-922Sk fibroblasts were infected with MV in the absence or presence of TNF or IFN-β alone or TNF plus IFN-β. MV yields were determined by the standard plaque assay using BGMK cells at 48 h after infection. (C) CCD-922Sk fibroblasts were infected with the control MV (constructed with the same vector but no human TNF gene) or the recombinant MV expressing human TNF (MV-hTNF) in the absence or presence of IFN-β. The viral yields of both control MV and MV-hTNF were determined by the standard plaque assay using RK-13 cells at 48 h after infection. (D) CCD-922Sk fibroblasts were infected with EMCV in the absence or presence of IFN-β or TNF. EMCV quantities were titrated by the standard plaque assay using BHK cells at 48 h after infection. Data in (B), (C) and (D) represent mean +/− SD.
    Anti Human Tnf, supplied by Thermo Fisher, 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/anti human tnf/product/Thermo Fisher
    Average 97 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti human tnf - by Bioz Stars, 2021-06
    97/100 stars
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    93
    Thermo Fisher rabbit anti human c1q polyclonal antibody
    (A) Binding of human <t>C1q</t> and recombinant globular head modules, ghA, ghB, and ghC (10 µg/ml; 1 h incubation) to SKOV3 cells using immunofluorescence microscopy. Panel A shows the nucleus of the cells stained with Hoechst. Panel B shows the cells probed with anti-C1q (C1q) and anti-maltose-binding protein (MBP) (globular heads) <t>polyclonal</t> antibodies, followed by anti-rabbit IgG labeled with FITC; the bound proteins are visible on the cell membrane (panels C and D). (B) Flow cytometric analysis to show binding of human C1q and ghA, ghB, and ghC (10 µg/ml) to SKOV3 cells after 1 h incubation. Panel a shows the number of cells probed with anti-C1q (C1q) and anti-MBP (globular heads) antibodies followed by anti-rabbit IgG labeled with FITC, as compared to the untreated cells. Panel b shows the shift in the fluorescent intensity from untreated to treated cells.
    Rabbit Anti Human C1q Polyclonal Antibody, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 93 stars, based on 1 article reviews
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    93
    Thermo Fisher anti human tnf α
    'Psoriasis 1' inhibited inflammatory response following VDR-siRNA transfection. T lymphocytes were isolated from patients with psoriasis and transfected with NC or VDR siRNA. Effects of high-dose 'Psoriasis 1' and triptolide on the levels of (A) <t>TNF-α,</t> (B) IFN-γ, (C) IL-2, (D) IL-6, (E) TGF-β, (F) IL-4, (G) IL-23, (H) IL-17 and (I) VD in T lymphocytes after VDR-siRNA transfection. Data are presented as mean ± standard deviation. ** P
    Anti Human Tnf α, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Thermo Fisher apc anti human tnf α
    Siglec-9 blockade restores cytokine secretion and degranulation of NK cells in chronic hepatitis B (CHB) patients. PBMCs from CHB patients pretreated with Siglec-9 blocking antibody or isotype control IgG were stimulated with PMA plus ionomycin. Then, the expression of IFN-γ (A) , <t>TNF-α</t> (B) , and CD107a (C) were analyzed by flow cytometry. The right panels showed the representative flow cytometry data from one subject.
    Apc Anti Human Tnf α, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    TNF and IFN-β are required for potent restriction of MV infection in primary human fibroblasts. (A) Primary human skin fibroblasts CCD-922Sk were mock-infected or infected with MV. X-gal staining was performed to visualize blue MV foci 48 h after infection. (B) CCD-922Sk fibroblasts were infected with MV in the absence or presence of TNF or IFN-β alone or TNF plus IFN-β. MV yields were determined by the standard plaque assay using BGMK cells at 48 h after infection. (C) CCD-922Sk fibroblasts were infected with the control MV (constructed with the same vector but no human TNF gene) or the recombinant MV expressing human TNF (MV-hTNF) in the absence or presence of IFN-β. The viral yields of both control MV and MV-hTNF were determined by the standard plaque assay using RK-13 cells at 48 h after infection. (D) CCD-922Sk fibroblasts were infected with EMCV in the absence or presence of IFN-β or TNF. EMCV quantities were titrated by the standard plaque assay using BHK cells at 48 h after infection. Data in (B), (C) and (D) represent mean +/− SD.

    Journal: PLoS Pathogens

    Article Title: RIG-I Mediates the Co-Induction of Tumor Necrosis Factor and Type I Interferon Elicited by Myxoma Virus in Primary Human Macrophages

    doi: 10.1371/journal.ppat.1000099

    Figure Lengend Snippet: TNF and IFN-β are required for potent restriction of MV infection in primary human fibroblasts. (A) Primary human skin fibroblasts CCD-922Sk were mock-infected or infected with MV. X-gal staining was performed to visualize blue MV foci 48 h after infection. (B) CCD-922Sk fibroblasts were infected with MV in the absence or presence of TNF or IFN-β alone or TNF plus IFN-β. MV yields were determined by the standard plaque assay using BGMK cells at 48 h after infection. (C) CCD-922Sk fibroblasts were infected with the control MV (constructed with the same vector but no human TNF gene) or the recombinant MV expressing human TNF (MV-hTNF) in the absence or presence of IFN-β. The viral yields of both control MV and MV-hTNF were determined by the standard plaque assay using RK-13 cells at 48 h after infection. (D) CCD-922Sk fibroblasts were infected with EMCV in the absence or presence of IFN-β or TNF. EMCV quantities were titrated by the standard plaque assay using BHK cells at 48 h after infection. Data in (B), (C) and (D) represent mean +/− SD.

    Article Snippet: The primary antibodies were obtained from the following suppliers: anti-IRF3, anti-IRF7, anti-NF-κB p65 and anti-USF2 antibodies, Santa Cruz Biotechnology; anti-human TNF and anti-human IFN-α/β antibodies, Biosource International; anti-β-actin antibody, Sigma; anti-STAT1 antibody, Transduction Laboratories.

    Techniques: Infection, Staining, Plaque Assay, Construct, Plasmid Preparation, Recombinant, Expressing

    MV-elicited production of TNF and IFN-β is mediated by RIG-I in primary human macrophages. (A) pHMs were transfected with control siRNA or siRNAs targeting cytoplasmic RNA sensors RIG-I (top panel) or MDA5 (middle panel). The cells were analyzed 48 h later by RT-PCR for the indicated mRNA levels. GAPDH was used as control. (B, C) RIG-I is critically required for MV-elicited production of both TNF (B) and IFN-β (C) in pHMs. pHMs or various siRNA pHMs were mock-infected or infected with MV and the accumulation of TNF and IFN-β in the culture supernatants was assessed by ELISA 24 h post-infection. (D) RIG-I mediates cellular restriction to MV infection in pHMs. pHMs or control siRNA or RIG-I siRNA pHMs as indicated were infected with MV. MV yields were determined by the standard plaque assay using BGMK cells at 48 h after infection. Data in (B), (C) and (D) represent mean +/− SD.

    Journal: PLoS Pathogens

    Article Title: RIG-I Mediates the Co-Induction of Tumor Necrosis Factor and Type I Interferon Elicited by Myxoma Virus in Primary Human Macrophages

    doi: 10.1371/journal.ppat.1000099

    Figure Lengend Snippet: MV-elicited production of TNF and IFN-β is mediated by RIG-I in primary human macrophages. (A) pHMs were transfected with control siRNA or siRNAs targeting cytoplasmic RNA sensors RIG-I (top panel) or MDA5 (middle panel). The cells were analyzed 48 h later by RT-PCR for the indicated mRNA levels. GAPDH was used as control. (B, C) RIG-I is critically required for MV-elicited production of both TNF (B) and IFN-β (C) in pHMs. pHMs or various siRNA pHMs were mock-infected or infected with MV and the accumulation of TNF and IFN-β in the culture supernatants was assessed by ELISA 24 h post-infection. (D) RIG-I mediates cellular restriction to MV infection in pHMs. pHMs or control siRNA or RIG-I siRNA pHMs as indicated were infected with MV. MV yields were determined by the standard plaque assay using BGMK cells at 48 h after infection. Data in (B), (C) and (D) represent mean +/− SD.

    Article Snippet: The primary antibodies were obtained from the following suppliers: anti-IRF3, anti-IRF7, anti-NF-κB p65 and anti-USF2 antibodies, Santa Cruz Biotechnology; anti-human TNF and anti-human IFN-α/β antibodies, Biosource International; anti-β-actin antibody, Sigma; anti-STAT1 antibody, Transduction Laboratories.

    Techniques: Transfection, Reverse Transcription Polymerase Chain Reaction, Infection, Enzyme-linked Immunosorbent Assay, Plaque Assay

    Primary human macrophages produce TNF and IFN-β in response to MV infection. (A, B) Primary human macrophages (pHMs), CCD-922Sk fibroblasts and primary human lymphocytes were mock-infected or infected with MV. TNF (A) and IFN-β (B) accumulation in the culture supernatants was assessed by ELISA 24 h post-infection. (C) pHMs were mock-infected or infected with MV in the absence or presence of TNF neutralizing antibody (Ab) or IFN-α/β neutralizing Ab alone or TNF Ab plus IFN-α/β Ab as specified. MV β-gal activity was determined by measuring absorbance at 420 nm and normalized to the total cellular protein levels at 48 h after infection. (D) pHMs were infected with MV or UV-inactivated MV for various times (below lanes) and total RNA was analyzed by RT-PCR for induction of TNF and IFN-β mRNA. GAPDH was used as control. Data in (A), (B) and (C) represent mean +/− SD.

    Journal: PLoS Pathogens

    Article Title: RIG-I Mediates the Co-Induction of Tumor Necrosis Factor and Type I Interferon Elicited by Myxoma Virus in Primary Human Macrophages

    doi: 10.1371/journal.ppat.1000099

    Figure Lengend Snippet: Primary human macrophages produce TNF and IFN-β in response to MV infection. (A, B) Primary human macrophages (pHMs), CCD-922Sk fibroblasts and primary human lymphocytes were mock-infected or infected with MV. TNF (A) and IFN-β (B) accumulation in the culture supernatants was assessed by ELISA 24 h post-infection. (C) pHMs were mock-infected or infected with MV in the absence or presence of TNF neutralizing antibody (Ab) or IFN-α/β neutralizing Ab alone or TNF Ab plus IFN-α/β Ab as specified. MV β-gal activity was determined by measuring absorbance at 420 nm and normalized to the total cellular protein levels at 48 h after infection. (D) pHMs were infected with MV or UV-inactivated MV for various times (below lanes) and total RNA was analyzed by RT-PCR for induction of TNF and IFN-β mRNA. GAPDH was used as control. Data in (A), (B) and (C) represent mean +/− SD.

    Article Snippet: The primary antibodies were obtained from the following suppliers: anti-IRF3, anti-IRF7, anti-NF-κB p65 and anti-USF2 antibodies, Santa Cruz Biotechnology; anti-human TNF and anti-human IFN-α/β antibodies, Biosource International; anti-β-actin antibody, Sigma; anti-STAT1 antibody, Transduction Laboratories.

    Techniques: Infection, Enzyme-linked Immunosorbent Assay, Activity Assay, Reverse Transcription Polymerase Chain Reaction

    IRF7 is crucial for sustaining MV-elicited TNF induction in primary human macrophages. (A) Control siRNA pHMs or IRF7 siRNA pHMs were infected with MV for various times (below lanes) and the whole cell lysates were analyzed for MV-induced expression of IRF7 protein. β-actin was used as control. (B) pHMs or various siRNA pHMs were mock-infected or infected with MV. TNF protein in the culture supernatants was assessed by ELISA 24 h post-infection. (C) IRF7 expression and TNF production kinetics. Control siRNA pHMs or IRF7 siRNA pHMs were infected with MV for various times as indicated and TNF protein in the culture supernatants was assessed by ELISA. (D) IRF7 is required for sustaining TNF gene transcription activated by MV infection. Control siRNA pHMs or IRF7 siRNA pHMs were infected with MV for various times (below lanes) and the cells were analyzed by RT-PCR for the indicated TNF mRNA levels. GAPDH was used as control. Data in (B) and (C) represent mean +/− SD.

    Journal: PLoS Pathogens

    Article Title: RIG-I Mediates the Co-Induction of Tumor Necrosis Factor and Type I Interferon Elicited by Myxoma Virus in Primary Human Macrophages

    doi: 10.1371/journal.ppat.1000099

    Figure Lengend Snippet: IRF7 is crucial for sustaining MV-elicited TNF induction in primary human macrophages. (A) Control siRNA pHMs or IRF7 siRNA pHMs were infected with MV for various times (below lanes) and the whole cell lysates were analyzed for MV-induced expression of IRF7 protein. β-actin was used as control. (B) pHMs or various siRNA pHMs were mock-infected or infected with MV. TNF protein in the culture supernatants was assessed by ELISA 24 h post-infection. (C) IRF7 expression and TNF production kinetics. Control siRNA pHMs or IRF7 siRNA pHMs were infected with MV for various times as indicated and TNF protein in the culture supernatants was assessed by ELISA. (D) IRF7 is required for sustaining TNF gene transcription activated by MV infection. Control siRNA pHMs or IRF7 siRNA pHMs were infected with MV for various times (below lanes) and the cells were analyzed by RT-PCR for the indicated TNF mRNA levels. GAPDH was used as control. Data in (B) and (C) represent mean +/− SD.

    Article Snippet: The primary antibodies were obtained from the following suppliers: anti-IRF3, anti-IRF7, anti-NF-κB p65 and anti-USF2 antibodies, Santa Cruz Biotechnology; anti-human TNF and anti-human IFN-α/β antibodies, Biosource International; anti-β-actin antibody, Sigma; anti-STAT1 antibody, Transduction Laboratories.

    Techniques: Infection, Expressing, Enzyme-linked Immunosorbent Assay, Reverse Transcription Polymerase Chain Reaction

    IRF3 is critical for triggering MV-elicited TNF induction in primary human macrophages. (A) pHMs were transfected with control siRNA or MAVS siRNA. The cells were analyzed 48 h later by RT-PCR for the indicated mRNA levels. GAPDH was used as the control. (B) Control siRNA pHMs or RIG-I siRNA or MAVS siRNA pHMs as indicated were infected with MV for various times (below lanes) and the nuclear extracts were probed for nuclear IRF3 (nuc-IRF3). Nuclear USF2 (nuc-USF2) was used as nuclear protein loading control. (C) Control siRNA pHMs or RIG-I siRNA or MAVS siRNA pHMs as indicated were infected with MV for 0 h or 10 h and were immunofluorescence-stained for IRF3 (red). Nuclear DNA was counterstained with DAPI (blue). Bars are 10 µm. (D) pHMs were transfected with control siRNA or IRF3 siRNA as indicated and were analyzed 72 h later by immunoblotting for IRF3 protein levels. β-actin was used as control. (E) pHMs or various siRNA pHMs as indicated were infected with MV for 24 h and TNF protein in the culture supernatants was assessed by ELISA. Data represent mean +/− SD. (F) Control siRNA pHMs or IRF3 siRNA pHMs were infected with MV for various times (below lanes) and the cells were analyzed by RT-PCR for the indicated TNF mRNA levels. GAPDH was used as control.

    Journal: PLoS Pathogens

    Article Title: RIG-I Mediates the Co-Induction of Tumor Necrosis Factor and Type I Interferon Elicited by Myxoma Virus in Primary Human Macrophages

    doi: 10.1371/journal.ppat.1000099

    Figure Lengend Snippet: IRF3 is critical for triggering MV-elicited TNF induction in primary human macrophages. (A) pHMs were transfected with control siRNA or MAVS siRNA. The cells were analyzed 48 h later by RT-PCR for the indicated mRNA levels. GAPDH was used as the control. (B) Control siRNA pHMs or RIG-I siRNA or MAVS siRNA pHMs as indicated were infected with MV for various times (below lanes) and the nuclear extracts were probed for nuclear IRF3 (nuc-IRF3). Nuclear USF2 (nuc-USF2) was used as nuclear protein loading control. (C) Control siRNA pHMs or RIG-I siRNA or MAVS siRNA pHMs as indicated were infected with MV for 0 h or 10 h and were immunofluorescence-stained for IRF3 (red). Nuclear DNA was counterstained with DAPI (blue). Bars are 10 µm. (D) pHMs were transfected with control siRNA or IRF3 siRNA as indicated and were analyzed 72 h later by immunoblotting for IRF3 protein levels. β-actin was used as control. (E) pHMs or various siRNA pHMs as indicated were infected with MV for 24 h and TNF protein in the culture supernatants was assessed by ELISA. Data represent mean +/− SD. (F) Control siRNA pHMs or IRF3 siRNA pHMs were infected with MV for various times (below lanes) and the cells were analyzed by RT-PCR for the indicated TNF mRNA levels. GAPDH was used as control.

    Article Snippet: The primary antibodies were obtained from the following suppliers: anti-IRF3, anti-IRF7, anti-NF-κB p65 and anti-USF2 antibodies, Santa Cruz Biotechnology; anti-human TNF and anti-human IFN-α/β antibodies, Biosource International; anti-β-actin antibody, Sigma; anti-STAT1 antibody, Transduction Laboratories.

    Techniques: Transfection, Reverse Transcription Polymerase Chain Reaction, Infection, Immunofluorescence, Staining, Enzyme-linked Immunosorbent Assay

    (A) Binding of human C1q and recombinant globular head modules, ghA, ghB, and ghC (10 µg/ml; 1 h incubation) to SKOV3 cells using immunofluorescence microscopy. Panel A shows the nucleus of the cells stained with Hoechst. Panel B shows the cells probed with anti-C1q (C1q) and anti-maltose-binding protein (MBP) (globular heads) polyclonal antibodies, followed by anti-rabbit IgG labeled with FITC; the bound proteins are visible on the cell membrane (panels C and D). (B) Flow cytometric analysis to show binding of human C1q and ghA, ghB, and ghC (10 µg/ml) to SKOV3 cells after 1 h incubation. Panel a shows the number of cells probed with anti-C1q (C1q) and anti-MBP (globular heads) antibodies followed by anti-rabbit IgG labeled with FITC, as compared to the untreated cells. Panel b shows the shift in the fluorescent intensity from untreated to treated cells.

    Journal: Frontiers in Immunology

    Article Title: Human C1q Induces Apoptosis in an Ovarian Cancer Cell Line via Tumor Necrosis Factor Pathway

    doi: 10.3389/fimmu.2016.00599

    Figure Lengend Snippet: (A) Binding of human C1q and recombinant globular head modules, ghA, ghB, and ghC (10 µg/ml; 1 h incubation) to SKOV3 cells using immunofluorescence microscopy. Panel A shows the nucleus of the cells stained with Hoechst. Panel B shows the cells probed with anti-C1q (C1q) and anti-maltose-binding protein (MBP) (globular heads) polyclonal antibodies, followed by anti-rabbit IgG labeled with FITC; the bound proteins are visible on the cell membrane (panels C and D). (B) Flow cytometric analysis to show binding of human C1q and ghA, ghB, and ghC (10 µg/ml) to SKOV3 cells after 1 h incubation. Panel a shows the number of cells probed with anti-C1q (C1q) and anti-MBP (globular heads) antibodies followed by anti-rabbit IgG labeled with FITC, as compared to the untreated cells. Panel b shows the shift in the fluorescent intensity from untreated to treated cells.

    Article Snippet: Cells were incubated at 4°C for 1 h, followed by 1 h incubation with rabbit anti-human C1q polyclonal antibody (1:200) for C1q and rabbit anti-MBP (Thermo Fisher, 1:200) for globular head modules treated cells as well as their respective BSA-treated controls.

    Techniques: Binding Assay, Recombinant, Incubation, Immunofluorescence, Microscopy, Staining, Labeling, Flow Cytometry

    'Psoriasis 1' inhibited inflammatory response following VDR-siRNA transfection. T lymphocytes were isolated from patients with psoriasis and transfected with NC or VDR siRNA. Effects of high-dose 'Psoriasis 1' and triptolide on the levels of (A) TNF-α, (B) IFN-γ, (C) IL-2, (D) IL-6, (E) TGF-β, (F) IL-4, (G) IL-23, (H) IL-17 and (I) VD in T lymphocytes after VDR-siRNA transfection. Data are presented as mean ± standard deviation. ** P

    Journal: International Journal of Molecular Medicine

    Article Title: 'Psoriasis 1' reduces T-lymphocyte-mediated inflammation in patients with psoriasis by inhibiting vitamin D receptor-mediated STAT4 inactivation

    doi: 10.3892/ijmm.2020.4695

    Figure Lengend Snippet: 'Psoriasis 1' inhibited inflammatory response following VDR-siRNA transfection. T lymphocytes were isolated from patients with psoriasis and transfected with NC or VDR siRNA. Effects of high-dose 'Psoriasis 1' and triptolide on the levels of (A) TNF-α, (B) IFN-γ, (C) IL-2, (D) IL-6, (E) TGF-β, (F) IL-4, (G) IL-23, (H) IL-17 and (I) VD in T lymphocytes after VDR-siRNA transfection. Data are presented as mean ± standard deviation. ** P

    Article Snippet: PE anti-human CD3 (cat. no. 300307-1), APC anti-human CD4 (cat. no. 317415-1), and FITC anti-human CD8 (cat. no. 344703-1) were obtained from BioLegend, Inc. RPMI-1640 medium and FBS were obtained from Invitrogen; Thermo Fisher Scientific, Inc. Anti-human TNF-α (cat. no. STA00D), IFN-γ (cat. no. SIF50), IL-2 (cat. no. S2050), IL-6 (cat. no. S6050), TGF-β (cat. no. SB100B), IL-4 (cat. no. S4050), IL-12 (cat. no. 10018-IL), IL-23 (cat. no. S2300B) and VD (cat. no. DVDBP0B) ELISA kits were supplied by R & D Systems, Inc.

    Techniques: Transfection, Isolation, Standard Deviation

    'Psoriasis 1' inhibits VDR-mediated STAT4 inactivation. (A and B) Effects of different doses of 'Psoriasis 1' and triptolide on the mRNA and protein expressions of VDR and STAT4 in T lymphocytes. (C) ELISA was performed to confirm the levels of IL-17A, TNF-α and IL-22. Data are presented as mean ± standard deviation. * P

    Journal: International Journal of Molecular Medicine

    Article Title: 'Psoriasis 1' reduces T-lymphocyte-mediated inflammation in patients with psoriasis by inhibiting vitamin D receptor-mediated STAT4 inactivation

    doi: 10.3892/ijmm.2020.4695

    Figure Lengend Snippet: 'Psoriasis 1' inhibits VDR-mediated STAT4 inactivation. (A and B) Effects of different doses of 'Psoriasis 1' and triptolide on the mRNA and protein expressions of VDR and STAT4 in T lymphocytes. (C) ELISA was performed to confirm the levels of IL-17A, TNF-α and IL-22. Data are presented as mean ± standard deviation. * P

    Article Snippet: PE anti-human CD3 (cat. no. 300307-1), APC anti-human CD4 (cat. no. 317415-1), and FITC anti-human CD8 (cat. no. 344703-1) were obtained from BioLegend, Inc. RPMI-1640 medium and FBS were obtained from Invitrogen; Thermo Fisher Scientific, Inc. Anti-human TNF-α (cat. no. STA00D), IFN-γ (cat. no. SIF50), IL-2 (cat. no. S2050), IL-6 (cat. no. S6050), TGF-β (cat. no. SB100B), IL-4 (cat. no. S4050), IL-12 (cat. no. 10018-IL), IL-23 (cat. no. S2300B) and VD (cat. no. DVDBP0B) ELISA kits were supplied by R & D Systems, Inc.

    Techniques: Enzyme-linked Immunosorbent Assay, Standard Deviation

    'Psoriasis 1' inhibits inflammatory response in T lymphocytes. Effects of 'Psoriasis 1' at different doses and triptolide on the levels of (A) TNF-α, (B) IFN-γ, (C) IL-2, (D) IL-6, (E) TGF-β, (F) IL-4, (G) IL-23, (H) IL-17 and (I) VD in T lymphocytes. Data are presented as mean ± standard deviation. * P

    Journal: International Journal of Molecular Medicine

    Article Title: 'Psoriasis 1' reduces T-lymphocyte-mediated inflammation in patients with psoriasis by inhibiting vitamin D receptor-mediated STAT4 inactivation

    doi: 10.3892/ijmm.2020.4695

    Figure Lengend Snippet: 'Psoriasis 1' inhibits inflammatory response in T lymphocytes. Effects of 'Psoriasis 1' at different doses and triptolide on the levels of (A) TNF-α, (B) IFN-γ, (C) IL-2, (D) IL-6, (E) TGF-β, (F) IL-4, (G) IL-23, (H) IL-17 and (I) VD in T lymphocytes. Data are presented as mean ± standard deviation. * P

    Article Snippet: PE anti-human CD3 (cat. no. 300307-1), APC anti-human CD4 (cat. no. 317415-1), and FITC anti-human CD8 (cat. no. 344703-1) were obtained from BioLegend, Inc. RPMI-1640 medium and FBS were obtained from Invitrogen; Thermo Fisher Scientific, Inc. Anti-human TNF-α (cat. no. STA00D), IFN-γ (cat. no. SIF50), IL-2 (cat. no. S2050), IL-6 (cat. no. S6050), TGF-β (cat. no. SB100B), IL-4 (cat. no. S4050), IL-12 (cat. no. 10018-IL), IL-23 (cat. no. S2300B) and VD (cat. no. DVDBP0B) ELISA kits were supplied by R & D Systems, Inc.

    Techniques: Standard Deviation

    Siglec-9 blockade restores cytokine secretion and degranulation of NK cells in chronic hepatitis B (CHB) patients. PBMCs from CHB patients pretreated with Siglec-9 blocking antibody or isotype control IgG were stimulated with PMA plus ionomycin. Then, the expression of IFN-γ (A) , TNF-α (B) , and CD107a (C) were analyzed by flow cytometry. The right panels showed the representative flow cytometry data from one subject.

    Journal: Frontiers in Immunology

    Article Title: Decreased Siglec-9 Expression on Natural Killer Cell Subset Associated With Persistent HBV Replication

    doi: 10.3389/fimmu.2018.01124

    Figure Lengend Snippet: Siglec-9 blockade restores cytokine secretion and degranulation of NK cells in chronic hepatitis B (CHB) patients. PBMCs from CHB patients pretreated with Siglec-9 blocking antibody or isotype control IgG were stimulated with PMA plus ionomycin. Then, the expression of IFN-γ (A) , TNF-α (B) , and CD107a (C) were analyzed by flow cytometry. The right panels showed the representative flow cytometry data from one subject.

    Article Snippet: For Siglec-9 blockade assay, PBMCs were preincubated with human Siglec-9 antibody with a final concentration of 10 µg/ml or IgG controls (R & D, Minneapolis, MN, USA) for 40 min and then stimulated with PMA (50 ng/ml) (SIGMA, St. Louis, MO, USA), ionomycin (1 µg/ml) (BioLegend, San Diego, CA, USA), and Brefeldin A (10 µg/ml) (BioLegend, San Diego, CA, USA) for 4 h. After incubation with PerCp/cy5.5 anti-human CD3, PE/Cy7 anti-human CD56, cells were treated with the permeable agent Cytofix/Cytoperm (eBioscience, San Diego, CA, USA) according to the manufacturer’s instructions and were intracellularly stained with FITC anti-human IFN-γ (Miltenyi Biotech GmbH, Bergisch Gladbach, Germany) or APC anti-human TNF-α (eBioscience, San Diego, CA, USA) for 30 min.

    Techniques: Blocking Assay, Expressing, Flow Cytometry, Cytometry

    Upregulated expression of Siglec-9 ligand in HBV infection and inflammatory milieu. (A) Detection of Siglec-9 ligand in liver biopsies from chronic hepatitis B (CHB) patients or normal liver tissues by immunofluorescence using Siglec-9-Fc chimera protein. (B,C) Expression of Siglec-9 ligand and hepatitis B surface antigen (HBsAg) in hepatoma cell line HLCZ01 with or without HBV infection (B) , and Huh7 cells treated with 100 ng/ml IL-6 or TNF-α for 24 h (C) , was evaluated by immunofluorescence staining.

    Journal: Frontiers in Immunology

    Article Title: Decreased Siglec-9 Expression on Natural Killer Cell Subset Associated With Persistent HBV Replication

    doi: 10.3389/fimmu.2018.01124

    Figure Lengend Snippet: Upregulated expression of Siglec-9 ligand in HBV infection and inflammatory milieu. (A) Detection of Siglec-9 ligand in liver biopsies from chronic hepatitis B (CHB) patients or normal liver tissues by immunofluorescence using Siglec-9-Fc chimera protein. (B,C) Expression of Siglec-9 ligand and hepatitis B surface antigen (HBsAg) in hepatoma cell line HLCZ01 with or without HBV infection (B) , and Huh7 cells treated with 100 ng/ml IL-6 or TNF-α for 24 h (C) , was evaluated by immunofluorescence staining.

    Article Snippet: For Siglec-9 blockade assay, PBMCs were preincubated with human Siglec-9 antibody with a final concentration of 10 µg/ml or IgG controls (R & D, Minneapolis, MN, USA) for 40 min and then stimulated with PMA (50 ng/ml) (SIGMA, St. Louis, MO, USA), ionomycin (1 µg/ml) (BioLegend, San Diego, CA, USA), and Brefeldin A (10 µg/ml) (BioLegend, San Diego, CA, USA) for 4 h. After incubation with PerCp/cy5.5 anti-human CD3, PE/Cy7 anti-human CD56, cells were treated with the permeable agent Cytofix/Cytoperm (eBioscience, San Diego, CA, USA) according to the manufacturer’s instructions and were intracellularly stained with FITC anti-human IFN-γ (Miltenyi Biotech GmbH, Bergisch Gladbach, Germany) or APC anti-human TNF-α (eBioscience, San Diego, CA, USA) for 30 min.

    Techniques: Expressing, Infection, Immunofluorescence, Staining