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anti fcγriii antibody  (R&D Systems)


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    R&D Systems anti fcγriii antibody
    ( A ) Recombinant mouse FcγRI, FcγRIIB, <t>FcγRIII,</t> FcγRIV, or the M2e-CS peptide was used as a coating antigen. WT M2e-mAb clone 602 and clone 602 with either the LE, LEEA2KA, or LALAPG Fc domain mutation (50 μg/ml) were used to determine binding to recombinant FcRs or the M2e-CS peptide by direct ELISA. PBS was used as a control. To test the binding of the WT and Fc-mutant M2e-mAb clone 602 preparations to C1q, the WT or mutant antibodies were used as coating antigens, followed by mouse C1q protein. PBS was used as a control. Anti-mouse C1q-biotin and avidin–horseradish peroxidase (HRP) were then used to quantify C1q protein bound by the capture antibodies by indirect ELISA. N = 3 independent experiments. ( B ) Summary of the differential binding affinities as determined in (A). ( C ) Experimental outline: Groups of 6- to 8-week-old female BALB/c mice were prophylactically intraperitoneally injected with either the WT (IgG2a) or the indicated Fc-mutant M2e-mAbs (all clone 602) on day −1 (100 μg per mouse). Control mice received PBS. Additional groups of mice were intraperitoneally injected with blocking mAbs specific to FcγRIII (100 μg per mouse) and/or FcγRIV (200 μg per mouse) on days −2, 1, and 4 and additionally prophylactically treated with the M2e-mAb clone 602 with the LE mutation (100 μg per mouse, intraperitoneally) at day −1. All mice were challenged with a lethal dose (3× LD 50 ) of PR8 by aerosol inhalation on day 0, and ( D ) survival and ( E ) weight loss were monitored for 21 days postinfection. Statistical significance for weight loss is shown in the heatmap. N = 10 to 29 mice per group; * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; survival: log-rank Mantel-Cox test; weight loss: two-way ANOVA with Dunnett’s multiple comparisons test.
    Anti Fcγriii Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 43 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+mouse+fc%CE%B3riii/Mouse+Fc+gamma+RIII+(CD16)+Antibody/pmc12422200-286-27-35
    Average 93 stars, based on 43 article reviews
    anti fcγriii antibody - by Bioz Stars, 2026-11
    93/100 stars

    Images

    1) Product Images from "Non-neutralizing antibodies to influenza A matrix-protein-2-ectodomain are broadly effective therapeutics and resistant to viral escape mutations"

    Article Title: Non-neutralizing antibodies to influenza A matrix-protein-2-ectodomain are broadly effective therapeutics and resistant to viral escape mutations

    Journal: Science Advances

    doi: 10.1126/sciadv.adx3505

    ( A ) Recombinant mouse FcγRI, FcγRIIB, FcγRIII, FcγRIV, or the M2e-CS peptide was used as a coating antigen. WT M2e-mAb clone 602 and clone 602 with either the LE, LEEA2KA, or LALAPG Fc domain mutation (50 μg/ml) were used to determine binding to recombinant FcRs or the M2e-CS peptide by direct ELISA. PBS was used as a control. To test the binding of the WT and Fc-mutant M2e-mAb clone 602 preparations to C1q, the WT or mutant antibodies were used as coating antigens, followed by mouse C1q protein. PBS was used as a control. Anti-mouse C1q-biotin and avidin–horseradish peroxidase (HRP) were then used to quantify C1q protein bound by the capture antibodies by indirect ELISA. N = 3 independent experiments. ( B ) Summary of the differential binding affinities as determined in (A). ( C ) Experimental outline: Groups of 6- to 8-week-old female BALB/c mice were prophylactically intraperitoneally injected with either the WT (IgG2a) or the indicated Fc-mutant M2e-mAbs (all clone 602) on day −1 (100 μg per mouse). Control mice received PBS. Additional groups of mice were intraperitoneally injected with blocking mAbs specific to FcγRIII (100 μg per mouse) and/or FcγRIV (200 μg per mouse) on days −2, 1, and 4 and additionally prophylactically treated with the M2e-mAb clone 602 with the LE mutation (100 μg per mouse, intraperitoneally) at day −1. All mice were challenged with a lethal dose (3× LD 50 ) of PR8 by aerosol inhalation on day 0, and ( D ) survival and ( E ) weight loss were monitored for 21 days postinfection. Statistical significance for weight loss is shown in the heatmap. N = 10 to 29 mice per group; * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; survival: log-rank Mantel-Cox test; weight loss: two-way ANOVA with Dunnett’s multiple comparisons test.
    Figure Legend Snippet: ( A ) Recombinant mouse FcγRI, FcγRIIB, FcγRIII, FcγRIV, or the M2e-CS peptide was used as a coating antigen. WT M2e-mAb clone 602 and clone 602 with either the LE, LEEA2KA, or LALAPG Fc domain mutation (50 μg/ml) were used to determine binding to recombinant FcRs or the M2e-CS peptide by direct ELISA. PBS was used as a control. To test the binding of the WT and Fc-mutant M2e-mAb clone 602 preparations to C1q, the WT or mutant antibodies were used as coating antigens, followed by mouse C1q protein. PBS was used as a control. Anti-mouse C1q-biotin and avidin–horseradish peroxidase (HRP) were then used to quantify C1q protein bound by the capture antibodies by indirect ELISA. N = 3 independent experiments. ( B ) Summary of the differential binding affinities as determined in (A). ( C ) Experimental outline: Groups of 6- to 8-week-old female BALB/c mice were prophylactically intraperitoneally injected with either the WT (IgG2a) or the indicated Fc-mutant M2e-mAbs (all clone 602) on day −1 (100 μg per mouse). Control mice received PBS. Additional groups of mice were intraperitoneally injected with blocking mAbs specific to FcγRIII (100 μg per mouse) and/or FcγRIV (200 μg per mouse) on days −2, 1, and 4 and additionally prophylactically treated with the M2e-mAb clone 602 with the LE mutation (100 μg per mouse, intraperitoneally) at day −1. All mice were challenged with a lethal dose (3× LD 50 ) of PR8 by aerosol inhalation on day 0, and ( D ) survival and ( E ) weight loss were monitored for 21 days postinfection. Statistical significance for weight loss is shown in the heatmap. N = 10 to 29 mice per group; * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; survival: log-rank Mantel-Cox test; weight loss: two-way ANOVA with Dunnett’s multiple comparisons test.

    Techniques Used: Recombinant, Mutagenesis, Binding Assay, Direct ELISA, Control, Avidin-Biotin Assay, Indirect ELISA, Injection, Blocking Assay, Aerosol

    Related Articles

    Blocking Assay:

    Article Title: Immune complexes stimulate CCR7-dependent dendritic cell migration to lymph nodes
    Article Snippet: DCs were generated by culturing the monocytes for 6 days with human GM-CSF (100 ng ml −1 , PeproTech) in DMEM supplemented with 10% heat-inactivated calf serum. .. For murine FcγR blocking studies, anti-mouse FcγRIII (CD16, AF1960) or goat anti-mouse isotype control (AB-108-C both obtained from R&D Systems, Minneapolis, MN) were added to cells 1 hour prior to stimulation with IC (final concentration 1.5 μg ml −1 ). .. Similarly, the PI3K inhibitor (ZSTK474, Selleckchem, 100 nM) or Akt inhibitor (AKT-XI (3-Formylchromone thiosemicarbazone, Cu(II)Cl 2 Complex, FPA-124), Merck-Millipore, 2.5 μM) was added to DCs prior to addition of IC and cells and supernatants harvested at 24 hours.

    Control:

    Article Title: Immune complexes stimulate CCR7-dependent dendritic cell migration to lymph nodes
    Article Snippet: DCs were generated by culturing the monocytes for 6 days with human GM-CSF (100 ng ml −1 , PeproTech) in DMEM supplemented with 10% heat-inactivated calf serum. .. For murine FcγR blocking studies, anti-mouse FcγRIII (CD16, AF1960) or goat anti-mouse isotype control (AB-108-C both obtained from R&D Systems, Minneapolis, MN) were added to cells 1 hour prior to stimulation with IC (final concentration 1.5 μg ml −1 ). .. Similarly, the PI3K inhibitor (ZSTK474, Selleckchem, 100 nM) or Akt inhibitor (AKT-XI (3-Formylchromone thiosemicarbazone, Cu(II)Cl 2 Complex, FPA-124), Merck-Millipore, 2.5 μM) was added to DCs prior to addition of IC and cells and supernatants harvested at 24 hours.

    Article Title: IgG subclasses determine pathways of anaphylaxis in mice
    Article Snippet: .. TNP (21-31) -BSA was obtained from Santa Cruz, ABT-491 from Sigma-Aldrich; cetirizine DiHCl from Selleck Chemicals; anti-mouse FcγRIII (275003) from R&D Systems; rat IgG2b isotype control (LTF-2) from Bio X Cell. ..

    Concentration Assay:

    Article Title: Immune complexes stimulate CCR7-dependent dendritic cell migration to lymph nodes
    Article Snippet: DCs were generated by culturing the monocytes for 6 days with human GM-CSF (100 ng ml −1 , PeproTech) in DMEM supplemented with 10% heat-inactivated calf serum. .. For murine FcγR blocking studies, anti-mouse FcγRIII (CD16, AF1960) or goat anti-mouse isotype control (AB-108-C both obtained from R&D Systems, Minneapolis, MN) were added to cells 1 hour prior to stimulation with IC (final concentration 1.5 μg ml −1 ). .. Similarly, the PI3K inhibitor (ZSTK474, Selleckchem, 100 nM) or Akt inhibitor (AKT-XI (3-Formylchromone thiosemicarbazone, Cu(II)Cl 2 Complex, FPA-124), Merck-Millipore, 2.5 μM) was added to DCs prior to addition of IC and cells and supernatants harvested at 24 hours.



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    https://www.bioz.com/product/anti+mouse+fc%CE%B3riii/anti+cd56/pmc11143926-257-31-34
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    ( A ) Recombinant mouse FcγRI, FcγRIIB, FcγRIII, FcγRIV, or the M2e-CS peptide was used as a coating antigen. WT M2e-mAb clone 602 and clone 602 with either the LE, LEEA2KA, or LALAPG Fc domain mutation (50 μg/ml) were used to determine binding to recombinant FcRs or the M2e-CS peptide by direct ELISA. PBS was used as a control. To test the binding of the WT and Fc-mutant M2e-mAb clone 602 preparations to C1q, the WT or mutant antibodies were used as coating antigens, followed by mouse C1q protein. PBS was used as a control. Anti-mouse C1q-biotin and avidin–horseradish peroxidase (HRP) were then used to quantify C1q protein bound by the capture antibodies by indirect ELISA. N = 3 independent experiments. ( B ) Summary of the differential binding affinities as determined in (A). ( C ) Experimental outline: Groups of 6- to 8-week-old female BALB/c mice were prophylactically intraperitoneally injected with either the WT (IgG2a) or the indicated Fc-mutant M2e-mAbs (all clone 602) on day −1 (100 μg per mouse). Control mice received PBS. Additional groups of mice were intraperitoneally injected with blocking mAbs specific to FcγRIII (100 μg per mouse) and/or FcγRIV (200 μg per mouse) on days −2, 1, and 4 and additionally prophylactically treated with the M2e-mAb clone 602 with the LE mutation (100 μg per mouse, intraperitoneally) at day −1. All mice were challenged with a lethal dose (3× LD 50 ) of PR8 by aerosol inhalation on day 0, and ( D ) survival and ( E ) weight loss were monitored for 21 days postinfection. Statistical significance for weight loss is shown in the heatmap. N = 10 to 29 mice per group; * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; survival: log-rank Mantel-Cox test; weight loss: two-way ANOVA with Dunnett’s multiple comparisons test.

    Journal: Science Advances

    Article Title: Non-neutralizing antibodies to influenza A matrix-protein-2-ectodomain are broadly effective therapeutics and resistant to viral escape mutations

    doi: 10.1126/sciadv.adx3505

    Figure Lengend Snippet: ( A ) Recombinant mouse FcγRI, FcγRIIB, FcγRIII, FcγRIV, or the M2e-CS peptide was used as a coating antigen. WT M2e-mAb clone 602 and clone 602 with either the LE, LEEA2KA, or LALAPG Fc domain mutation (50 μg/ml) were used to determine binding to recombinant FcRs or the M2e-CS peptide by direct ELISA. PBS was used as a control. To test the binding of the WT and Fc-mutant M2e-mAb clone 602 preparations to C1q, the WT or mutant antibodies were used as coating antigens, followed by mouse C1q protein. PBS was used as a control. Anti-mouse C1q-biotin and avidin–horseradish peroxidase (HRP) were then used to quantify C1q protein bound by the capture antibodies by indirect ELISA. N = 3 independent experiments. ( B ) Summary of the differential binding affinities as determined in (A). ( C ) Experimental outline: Groups of 6- to 8-week-old female BALB/c mice were prophylactically intraperitoneally injected with either the WT (IgG2a) or the indicated Fc-mutant M2e-mAbs (all clone 602) on day −1 (100 μg per mouse). Control mice received PBS. Additional groups of mice were intraperitoneally injected with blocking mAbs specific to FcγRIII (100 μg per mouse) and/or FcγRIV (200 μg per mouse) on days −2, 1, and 4 and additionally prophylactically treated with the M2e-mAb clone 602 with the LE mutation (100 μg per mouse, intraperitoneally) at day −1. All mice were challenged with a lethal dose (3× LD 50 ) of PR8 by aerosol inhalation on day 0, and ( D ) survival and ( E ) weight loss were monitored for 21 days postinfection. Statistical significance for weight loss is shown in the heatmap. N = 10 to 29 mice per group; * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; survival: log-rank Mantel-Cox test; weight loss: two-way ANOVA with Dunnett’s multiple comparisons test.

    Article Snippet: To block the activities of FcγRIII and FcγRIV in vivo, BALB/c mice were intraperitoneally infused on days −2, 1, and 4 post–PR8 IAV infection with commercially available anti-FcγRIII antibody (100 μg per mouse; clone: 275003, R&D Systems) and/or anti-FcγRIV antibody (200 μg per mouse; clone: 9E9 BioLegend), based on a published protocol ( ).

    Techniques: Recombinant, Mutagenesis, Binding Assay, Direct ELISA, Control, Avidin-Biotin Assay, Indirect ELISA, Injection, Blocking Assay, Aerosol

    Fcγ receptor dependence for IgG uptake in the developing forebrain. A Fcγ receptor expression analysis using single-cell RNA-seq data from E7-E18.5 mouse brain. The “Immune” cluster is divided into 8 classes. The mRNA expression of Fcgrt, Fcgr1, and Fcgr3 in different types of microglia and macrophages is shown in violin plots. B FcγRI and FcγRIII protein expression in CX3CR1-GFP mice at E16.5. Scale bar: 100 μm. C , D Co-immunohistochemistry of P0 cerebral cortex. IgG signals on P2RY12-positive microglia and CD206-positive BAMs are nearly abolished in Fcer1g KO mice. Scale bar: 25 μm. E Immunohistochemistry of P0 mice. IgG signals are observed in the meninges as indicated by the arrowhead and axon bundles at the corpus callosum in Fcer1g KO mice. Scale bar: 100 μm

    Journal: Inflammation and Regeneration

    Article Title: Maternal immunoglobulins are distributed in the offspring’s brain to support the maintenance of cortical interneurons in the postnatal period

    doi: 10.1186/s41232-024-00336-3

    Figure Lengend Snippet: Fcγ receptor dependence for IgG uptake in the developing forebrain. A Fcγ receptor expression analysis using single-cell RNA-seq data from E7-E18.5 mouse brain. The “Immune” cluster is divided into 8 classes. The mRNA expression of Fcgrt, Fcgr1, and Fcgr3 in different types of microglia and macrophages is shown in violin plots. B FcγRI and FcγRIII protein expression in CX3CR1-GFP mice at E16.5. Scale bar: 100 μm. C , D Co-immunohistochemistry of P0 cerebral cortex. IgG signals on P2RY12-positive microglia and CD206-positive BAMs are nearly abolished in Fcer1g KO mice. Scale bar: 25 μm. E Immunohistochemistry of P0 mice. IgG signals are observed in the meninges as indicated by the arrowhead and axon bundles at the corpus callosum in Fcer1g KO mice. Scale bar: 100 μm

    Article Snippet: The primary antibodies used were anti-Iba1 antibody (1:1000, 019–19741, WAKO), anti-P2RY12 (purinergic receptor P2Y, G-protein coupled 12) antibody (1:1000, AS-55043A, Anaspec), anti-mannose receptor antibody (1:600, ab64693, abcam), anti-CD31 antibody (1:1000, ab119341, abcam), anti-PDGFRβ antibody (1:100, MA5-15143, Invitrogen), anti-mouse FcγRIII antibody (1:200, AF1960, R&D systems), PE anti-mouse CD64 (FcγRI) antibody (1:100, 164403, BioLegend), anti-somatostatin (SST) antibody (H-106) (1:500, sc-13099, abcam), anti-parvalbumin (PV) antibody (1:1000, P3088, SIGMA), and anti-reelin antibody (1:400, AF3820, R&D systems).

    Techniques: Expressing, RNA Sequencing, Immunohistochemistry