igg2a isotype control Search Results


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FIGURE 1. IL-1RI and TLR4 expression in bronchial epithelial cells. A, 16HBE14o cells (1 104/ml) were stained for IL-1RI with 10 g/ml mouse monoclonal anti-human IL-1RI or a mouse-conjugated IgG1 isotype control Ab and analyzed by laser scanning cytometry. B, 16HBE14o cells (1 104/ml) were stained for TLR4 with 10 g/ml mouse monoclonal anti-human TLR4 or a mouse conjugated <t>IgG2a</t> isotype control Ab and analyzed by laser scanning cytometry.
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FIGURE 1. IL-1RI and TLR4 expression in bronchial epithelial cells. A, 16HBE14o cells (1 104/ml) were stained for IL-1RI with 10 g/ml mouse monoclonal anti-human IL-1RI or a mouse-conjugated IgG1 isotype control Ab and analyzed by laser scanning cytometry. B, 16HBE14o cells (1 104/ml) were stained for TLR4 with 10 g/ml mouse monoclonal anti-human TLR4 or a mouse conjugated <t>IgG2a</t> isotype control Ab and analyzed by laser scanning cytometry.
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FIGURE 1. IL-1RI and TLR4 expression in bronchial epithelial cells. A, 16HBE14o cells (1 104/ml) were stained for IL-1RI with 10 g/ml mouse monoclonal anti-human IL-1RI or a mouse-conjugated IgG1 isotype control Ab and analyzed by laser scanning cytometry. B, 16HBE14o cells (1 104/ml) were stained for TLR4 with 10 g/ml mouse monoclonal anti-human TLR4 or a mouse conjugated <t>IgG2a</t> isotype control Ab and analyzed by laser scanning cytometry.
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R&D Systems igg2 a isotype control
FIGURE 1. IL-1RI and TLR4 expression in bronchial epithelial cells. A, 16HBE14o cells (1 104/ml) were stained for IL-1RI with 10 g/ml mouse monoclonal anti-human IL-1RI or a mouse-conjugated IgG1 isotype control Ab and analyzed by laser scanning cytometry. B, 16HBE14o cells (1 104/ml) were stained for TLR4 with 10 g/ml mouse monoclonal anti-human TLR4 or a mouse conjugated <t>IgG2a</t> isotype control Ab and analyzed by laser scanning cytometry.
Igg2 A Isotype Control, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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FIGURE 1. IL-1RI and TLR4 expression in bronchial epithelial cells. A, 16HBE14o cells (1 104/ml) were stained for IL-1RI with 10 g/ml mouse monoclonal anti-human IL-1RI or a mouse-conjugated IgG1 isotype control Ab and analyzed by laser scanning cytometry. B, 16HBE14o cells (1 104/ml) were stained for TLR4 with 10 g/ml mouse monoclonal anti-human TLR4 or a mouse conjugated <t>IgG2a</t> isotype control Ab and analyzed by laser scanning cytometry.
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FIGURE 1. IL-1RI and TLR4 expression in bronchial epithelial cells. A, 16HBE14o cells (1 104/ml) were stained for IL-1RI with 10 g/ml mouse monoclonal anti-human IL-1RI or a mouse-conjugated IgG1 isotype control Ab and analyzed by laser scanning cytometry. B, 16HBE14o cells (1 104/ml) were stained for TLR4 with 10 g/ml mouse monoclonal anti-human TLR4 or a mouse conjugated <t>IgG2a</t> isotype control Ab and analyzed by laser scanning cytometry.
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FIGURE 1. IL-1RI and TLR4 expression in bronchial epithelial cells. A, 16HBE14o cells (1 104/ml) were stained for IL-1RI with 10 g/ml mouse monoclonal anti-human IL-1RI or a mouse-conjugated IgG1 isotype control Ab and analyzed by laser scanning cytometry. B, 16HBE14o cells (1 104/ml) were stained for TLR4 with 10 g/ml mouse monoclonal anti-human TLR4 or a mouse conjugated <t>IgG2a</t> isotype control Ab and analyzed by laser scanning cytometry.
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FIGURE 1. IL-1RI and TLR4 expression in bronchial epithelial cells. A, 16HBE14o cells (1 104/ml) were stained for IL-1RI with 10 g/ml mouse monoclonal anti-human IL-1RI or a mouse-conjugated IgG1 isotype control Ab and analyzed by laser scanning cytometry. B, 16HBE14o cells (1 104/ml) were stained for TLR4 with 10 g/ml mouse monoclonal anti-human TLR4 or a mouse conjugated <t>IgG2a</t> isotype control Ab and analyzed by laser scanning cytometry.
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WT mice were placed on standard diet (SD) or 60% high-fat diet (HFD) for a minimum of 12 weeks. (A-K) WT and HFD mice were inoculated by intranasal (IN) infection with 1000 tissue culture infectious dose-50 (TCID 50 ) of A/California/04/2009 (CA/09 H1N1) virus or PBS as a mock control. (A-E) NK cells were depleted with 300 μg of anti-NK1.1 PK136 antibody or an <t>IgG2a</t> isotype control days -2, -1, day of infection (d0), +1, and then every other day throughout the duration of the experiment. (A) Graphical summary and timeline of NK cell depletion studies made with Biorender (B) Probability of survival and median day survival time (n=9-10 per group ) and (C) Clinical scores post-infection. (D) Lungs were harvested at 3 days-post infection (dpi) and viral titers were determined via TCID 50 ( n=4-5 per group) (E) Representative gross lung images at 3 dpi with black arrows indicating areas of pulmonary hemorrhage. (F, I-K) At 1- or 3-dpi lungs were resected and processed for flow cytometry. Single-cell suspensions were stained for surface antibodies to characterize natural killer (NK) cells. (F) Number per 10 5 lung cells of NK cells (CD45 + , TCRβ - , NK1.1 + ) ( n=4-10 per group) (G) Lungs were processed for immunofluorescence at 3 dpi and stained for DAPI (blue), influenza NP protein (red) and NKp46 (NK cell marker, green) and (H) Number of NK cells per 250 2 μm was quantified. (I) Average expression of the NK cell markers CD27 and CD11b to assess maturation stage. (J) Frequency of CD11b + CD27 - lung NK cells and (K) Frequency of CD11b + CD27 + lung NK cells at baseline or at 1 or 3 dpi ( n=4-7 per group). Data are shown as mean ± SEM. Statistical significance was calculated using Mantel-Cox log-rank analysis (A) a two-way ANOVA (C), a One-way ANOVA with multiple comparison’s test (D, F, J, K) and a students t test with Welch’s correction (H) , * p < .05; ** p < .01; **** p < .0001; ns = not significant.
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Fig. 3 | Passive transfer of immunity to T. vivax infections with anti-IFX antibodies. a, Dose-dependent inhibition of T. vivax by adoptive transfer of sera from IFX-vaccinated mice relative to sera from unimmunized control mice. Groups of five mice were compared by one-way analysis of variance (ANOVA) with Sidak post hoc test; *P ≤ 0.05, ****P ≤ 0.0001. b, Three out of six anti-IFX <t>IgG1-isotype</t> monoclonal antibodies (6B3, 8E12 and 3D12), each given at a dose of 3 × 100 μg, passively protect against T. vivax infection relative to an
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Fig. 3 | Passive transfer of immunity to T. vivax infections with anti-IFX antibodies. a, Dose-dependent inhibition of T. vivax by adoptive transfer of sera from IFX-vaccinated mice relative to sera from unimmunized control mice. Groups of five mice were compared by one-way analysis of variance (ANOVA) with Sidak post hoc test; *P ≤ 0.05, ****P ≤ 0.0001. b, Three out of six anti-IFX <t>IgG1-isotype</t> monoclonal antibodies (6B3, 8E12 and 3D12), each given at a dose of 3 × 100 μg, passively protect against T. vivax infection relative to an
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Fig. 3 | Passive transfer of immunity to T. vivax infections with anti-IFX antibodies. a, Dose-dependent inhibition of T. vivax by adoptive transfer of sera from IFX-vaccinated mice relative to sera from unimmunized control mice. Groups of five mice were compared by one-way analysis of variance (ANOVA) with Sidak post hoc test; *P ≤ 0.05, ****P ≤ 0.0001. b, Three out of six anti-IFX <t>IgG1-isotype</t> monoclonal antibodies (6B3, 8E12 and 3D12), each given at a dose of 3 × 100 μg, passively protect against T. vivax infection relative to an
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Image Search Results


FIGURE 1. IL-1RI and TLR4 expression in bronchial epithelial cells. A, 16HBE14o cells (1 104/ml) were stained for IL-1RI with 10 g/ml mouse monoclonal anti-human IL-1RI or a mouse-conjugated IgG1 isotype control Ab and analyzed by laser scanning cytometry. B, 16HBE14o cells (1 104/ml) were stained for TLR4 with 10 g/ml mouse monoclonal anti-human TLR4 or a mouse conjugated IgG2a isotype control Ab and analyzed by laser scanning cytometry.

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

Article Title: Viral inhibition of IL-1- and neutrophil elastase-induced inflammatory responses in bronchial epithelial cells.

doi: 10.4049/jimmunol.175.11.7594

Figure Lengend Snippet: FIGURE 1. IL-1RI and TLR4 expression in bronchial epithelial cells. A, 16HBE14o cells (1 104/ml) were stained for IL-1RI with 10 g/ml mouse monoclonal anti-human IL-1RI or a mouse-conjugated IgG1 isotype control Ab and analyzed by laser scanning cytometry. B, 16HBE14o cells (1 104/ml) were stained for TLR4 with 10 g/ml mouse monoclonal anti-human TLR4 or a mouse conjugated IgG2a isotype control Ab and analyzed by laser scanning cytometry.

Article Snippet: Cells were Fc blocked with 1 g/ml goat IgG1 for 15 min at room temperature and labeled with 10 g/ml of a mAb directed against human IL-1RI (QED Bioscience), human TLR4 (Santa Cruz Biotechnology), or mouse IgG1 or IgG2a isotype control Abs (R&D Systems).

Techniques: Expressing, Staining, Control, Cytometry

WT mice were placed on standard diet (SD) or 60% high-fat diet (HFD) for a minimum of 12 weeks. (A-K) WT and HFD mice were inoculated by intranasal (IN) infection with 1000 tissue culture infectious dose-50 (TCID 50 ) of A/California/04/2009 (CA/09 H1N1) virus or PBS as a mock control. (A-E) NK cells were depleted with 300 μg of anti-NK1.1 PK136 antibody or an IgG2a isotype control days -2, -1, day of infection (d0), +1, and then every other day throughout the duration of the experiment. (A) Graphical summary and timeline of NK cell depletion studies made with Biorender (B) Probability of survival and median day survival time (n=9-10 per group ) and (C) Clinical scores post-infection. (D) Lungs were harvested at 3 days-post infection (dpi) and viral titers were determined via TCID 50 ( n=4-5 per group) (E) Representative gross lung images at 3 dpi with black arrows indicating areas of pulmonary hemorrhage. (F, I-K) At 1- or 3-dpi lungs were resected and processed for flow cytometry. Single-cell suspensions were stained for surface antibodies to characterize natural killer (NK) cells. (F) Number per 10 5 lung cells of NK cells (CD45 + , TCRβ - , NK1.1 + ) ( n=4-10 per group) (G) Lungs were processed for immunofluorescence at 3 dpi and stained for DAPI (blue), influenza NP protein (red) and NKp46 (NK cell marker, green) and (H) Number of NK cells per 250 2 μm was quantified. (I) Average expression of the NK cell markers CD27 and CD11b to assess maturation stage. (J) Frequency of CD11b + CD27 - lung NK cells and (K) Frequency of CD11b + CD27 + lung NK cells at baseline or at 1 or 3 dpi ( n=4-7 per group). Data are shown as mean ± SEM. Statistical significance was calculated using Mantel-Cox log-rank analysis (A) a two-way ANOVA (C), a One-way ANOVA with multiple comparison’s test (D, F, J, K) and a students t test with Welch’s correction (H) , * p < .05; ** p < .01; **** p < .0001; ns = not significant.

Journal: bioRxiv

Article Title: Obesity-Driven Lung Lipidome Remodeling Suppresses NK Cell Activation and Antiviral Immunity to Influenza Infection

doi: 10.64898/2026.03.06.710186

Figure Lengend Snippet: WT mice were placed on standard diet (SD) or 60% high-fat diet (HFD) for a minimum of 12 weeks. (A-K) WT and HFD mice were inoculated by intranasal (IN) infection with 1000 tissue culture infectious dose-50 (TCID 50 ) of A/California/04/2009 (CA/09 H1N1) virus or PBS as a mock control. (A-E) NK cells were depleted with 300 μg of anti-NK1.1 PK136 antibody or an IgG2a isotype control days -2, -1, day of infection (d0), +1, and then every other day throughout the duration of the experiment. (A) Graphical summary and timeline of NK cell depletion studies made with Biorender (B) Probability of survival and median day survival time (n=9-10 per group ) and (C) Clinical scores post-infection. (D) Lungs were harvested at 3 days-post infection (dpi) and viral titers were determined via TCID 50 ( n=4-5 per group) (E) Representative gross lung images at 3 dpi with black arrows indicating areas of pulmonary hemorrhage. (F, I-K) At 1- or 3-dpi lungs were resected and processed for flow cytometry. Single-cell suspensions were stained for surface antibodies to characterize natural killer (NK) cells. (F) Number per 10 5 lung cells of NK cells (CD45 + , TCRβ - , NK1.1 + ) ( n=4-10 per group) (G) Lungs were processed for immunofluorescence at 3 dpi and stained for DAPI (blue), influenza NP protein (red) and NKp46 (NK cell marker, green) and (H) Number of NK cells per 250 2 μm was quantified. (I) Average expression of the NK cell markers CD27 and CD11b to assess maturation stage. (J) Frequency of CD11b + CD27 - lung NK cells and (K) Frequency of CD11b + CD27 + lung NK cells at baseline or at 1 or 3 dpi ( n=4-7 per group). Data are shown as mean ± SEM. Statistical significance was calculated using Mantel-Cox log-rank analysis (A) a two-way ANOVA (C), a One-way ANOVA with multiple comparison’s test (D, F, J, K) and a students t test with Welch’s correction (H) , * p < .05; ** p < .01; **** p < .0001; ns = not significant.

Article Snippet: For in vivo NK cell depletion, mice were administered 300 μg anti-NK1.1 monoclonal antibody (PK136, BioXCell) or the corresponding InVivoPlus mouse IgG2a isotype control (BioXCell) by intraperitoneal injection -2, -1, day of infection, +1, then every other day until the conclusion of the experiment.

Techniques: Infection, Virus, Control, Flow Cytometry, Single Cell, Staining, Immunofluorescence, Marker, Expressing

WT mice were placed on standard diet (SD) or 60% high-fat diet (HFD) for a minimum of 12 weeks. SD and HFD mice were inoculated by intranasal (IN) infection with 1000 tissue culture infectious dose-50 (TCID 50 ) of A/California/04/2009 (CA/09 H1N1) virus or PBS as a mock control. (A-C) NK cells were depleted with 300 μg of anti-NK1.1 PK136 antibody or an IgG2a isotype control days -2, -1, day of infection (d0) and then lungs or spleens were resected and processed for flow cytometry. (A) Example gating of lung NK cells (B) Frequency and number of NK cells (CD45 + Tcrβ - NK1.1 + DX5 + ) assessed by flow cytometry in the lung and (C) in the spleen. (D) NK cells were depleted with 300 μg of anti-NK1.1 PK136 antibody or an IgG2a isotype control days -2, -1, day of infection (d0), +1, and then every other day throughout the duration of the experiment and weight loss over time was assessed. Data are shown as mean ± SD (B, C) or SEM (D) . Statistical significance was calculated using a One-way ANOVA with multiple comparison’s test (B, C) and a Two-way ANOVA (D) , ** p < .01; *** p < .001; **** p < .0001; ns = not significant.

Journal: bioRxiv

Article Title: Obesity-Driven Lung Lipidome Remodeling Suppresses NK Cell Activation and Antiviral Immunity to Influenza Infection

doi: 10.64898/2026.03.06.710186

Figure Lengend Snippet: WT mice were placed on standard diet (SD) or 60% high-fat diet (HFD) for a minimum of 12 weeks. SD and HFD mice were inoculated by intranasal (IN) infection with 1000 tissue culture infectious dose-50 (TCID 50 ) of A/California/04/2009 (CA/09 H1N1) virus or PBS as a mock control. (A-C) NK cells were depleted with 300 μg of anti-NK1.1 PK136 antibody or an IgG2a isotype control days -2, -1, day of infection (d0) and then lungs or spleens were resected and processed for flow cytometry. (A) Example gating of lung NK cells (B) Frequency and number of NK cells (CD45 + Tcrβ - NK1.1 + DX5 + ) assessed by flow cytometry in the lung and (C) in the spleen. (D) NK cells were depleted with 300 μg of anti-NK1.1 PK136 antibody or an IgG2a isotype control days -2, -1, day of infection (d0), +1, and then every other day throughout the duration of the experiment and weight loss over time was assessed. Data are shown as mean ± SD (B, C) or SEM (D) . Statistical significance was calculated using a One-way ANOVA with multiple comparison’s test (B, C) and a Two-way ANOVA (D) , ** p < .01; *** p < .001; **** p < .0001; ns = not significant.

Article Snippet: For in vivo NK cell depletion, mice were administered 300 μg anti-NK1.1 monoclonal antibody (PK136, BioXCell) or the corresponding InVivoPlus mouse IgG2a isotype control (BioXCell) by intraperitoneal injection -2, -1, day of infection, +1, then every other day until the conclusion of the experiment.

Techniques: Infection, Virus, Control, Flow Cytometry

Fig. 3 | Passive transfer of immunity to T. vivax infections with anti-IFX antibodies. a, Dose-dependent inhibition of T. vivax by adoptive transfer of sera from IFX-vaccinated mice relative to sera from unimmunized control mice. Groups of five mice were compared by one-way analysis of variance (ANOVA) with Sidak post hoc test; *P ≤ 0.05, ****P ≤ 0.0001. b, Three out of six anti-IFX IgG1-isotype monoclonal antibodies (6B3, 8E12 and 3D12), each given at a dose of 3 × 100 μg, passively protect against T. vivax infection relative to an

Journal: Nature

Article Title: An invariant Trypanosoma vivax vaccine antigen induces protective immunity.

doi: 10.1038/s41586-021-03597-x

Figure Lengend Snippet: Fig. 3 | Passive transfer of immunity to T. vivax infections with anti-IFX antibodies. a, Dose-dependent inhibition of T. vivax by adoptive transfer of sera from IFX-vaccinated mice relative to sera from unimmunized control mice. Groups of five mice were compared by one-way analysis of variance (ANOVA) with Sidak post hoc test; *P ≤ 0.05, ****P ≤ 0.0001. b, Three out of six anti-IFX IgG1-isotype monoclonal antibodies (6B3, 8E12 and 3D12), each given at a dose of 3 × 100 μg, passively protect against T. vivax infection relative to an

Article Snippet: Mouse isotype control antibodies were: IgG1 (MOPC-21, BE0083, BioXcell) and IgG2a (C1.18.4, BE0085, BioXcell).

Techniques: Inhibition, Adoptive Transfer Assay, Control, Bioprocessing, Infection

Fig. 4 | There are several mechanisms of antibody-mediated anti-IFX immunological protection, dominated by complement recruitment. a, Anti-IFX 8E12–IgG2a monoclonal antibodies passively protect against T. vivax infection more potently than do 8E12–IgG1 monoclonal antibodies. b, Dose titration of 8E12–IgG2a monoclonal antibody compared to isotype-matched control. c, Passive transfer of 8E12–IgG2a monoclonal antibodies containing mutations that prevent binding to C1q (ΔC1q),

Journal: Nature

Article Title: An invariant Trypanosoma vivax vaccine antigen induces protective immunity.

doi: 10.1038/s41586-021-03597-x

Figure Lengend Snippet: Fig. 4 | There are several mechanisms of antibody-mediated anti-IFX immunological protection, dominated by complement recruitment. a, Anti-IFX 8E12–IgG2a monoclonal antibodies passively protect against T. vivax infection more potently than do 8E12–IgG1 monoclonal antibodies. b, Dose titration of 8E12–IgG2a monoclonal antibody compared to isotype-matched control. c, Passive transfer of 8E12–IgG2a monoclonal antibodies containing mutations that prevent binding to C1q (ΔC1q),

Article Snippet: Mouse isotype control antibodies were: IgG1 (MOPC-21, BE0083, BioXcell) and IgG2a (C1.18.4, BE0085, BioXcell).

Techniques: Bioprocessing, Infection, Titration, Control, Binding Assay