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Becton Dickinson ifnar-cd8α-pe-cy7 (53–6.7)
Loss of host IFNAR1 increases tumorigenesis and impairs host antitumor immunity. 1 × 105 EO771.LMB cells were injected into the fourth mammary fat pad (IMFP) of wild type (WT) and <t>Ifnar−/−</t> C57BL/6 mice (in which host IFNAR1 is deleted) at day 0 and subsequent alterations to circulating and primary tumor cells assessed. Peripheral blood (PB) was taken at day 7 for FACS analysis and for intracellular staining (ICS) of monocytes was performed at endpoint. Primary tumor a volume (mm3) from WT (n = 4); Ifnar−/− (n = 5) mice and b weights (mg) of WT (n = 7); Ifnar−/− (n = 6) mice at experimental endpoint. Flow cytometric analysis of PB c NK (NK1.1+) cell and d CD69+ NK cell frequency (%); WT (n = 7); Ifnar−/− (n = 6) e Absolute number (cell #) of primary tumor NK cells (n = 5/group). Flow cytometric analysis of primary tumor (n = 5/group) f CD69+ and g IFNγ+ NK cell frequency (%) (h representative flow cytometry plots shown), i NK cell IFNAR1 expression and j mCherry+ EO771.LMB Rae-1 expression, represented as MFI (mean fluorescence intensity). Flow cytometric analysis of primary tumor (n = 5/group) k. CD4+ T cells IFNAR1 expression, l CD4+ IFNγ+ T cells, m CD8+ T cells IFNAR1 expression and n CD8+ IFNγ+ T cells, represented as frequency (%). p values * < 0.05, ** < 0.005, *** < 0.0005. **** < 0.0001 determined by Student’s t test. Errors bars, SEM
Ifnar Cd8α Pe Cy7 (53–6.7), supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
ifnar-cd8α-pe-cy7 (53–6.7) - by Bioz Stars, 2026-04
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1) Product Images from "Loss of type I IFN responsiveness impairs natural killer cell antitumor activity in breast cancer"

Article Title: Loss of type I IFN responsiveness impairs natural killer cell antitumor activity in breast cancer

Journal: Cancer Immunology, Immunotherapy : CII

doi: 10.1007/s00262-021-02857-z

Loss of host IFNAR1 increases tumorigenesis and impairs host antitumor immunity. 1 × 105 EO771.LMB cells were injected into the fourth mammary fat pad (IMFP) of wild type (WT) and Ifnar−/− C57BL/6 mice (in which host IFNAR1 is deleted) at day 0 and subsequent alterations to circulating and primary tumor cells assessed. Peripheral blood (PB) was taken at day 7 for FACS analysis and for intracellular staining (ICS) of monocytes was performed at endpoint. Primary tumor a volume (mm3) from WT (n = 4); Ifnar−/− (n = 5) mice and b weights (mg) of WT (n = 7); Ifnar−/− (n = 6) mice at experimental endpoint. Flow cytometric analysis of PB c NK (NK1.1+) cell and d CD69+ NK cell frequency (%); WT (n = 7); Ifnar−/− (n = 6) e Absolute number (cell #) of primary tumor NK cells (n = 5/group). Flow cytometric analysis of primary tumor (n = 5/group) f CD69+ and g IFNγ+ NK cell frequency (%) (h representative flow cytometry plots shown), i NK cell IFNAR1 expression and j mCherry+ EO771.LMB Rae-1 expression, represented as MFI (mean fluorescence intensity). Flow cytometric analysis of primary tumor (n = 5/group) k. CD4+ T cells IFNAR1 expression, l CD4+ IFNγ+ T cells, m CD8+ T cells IFNAR1 expression and n CD8+ IFNγ+ T cells, represented as frequency (%). p values * < 0.05, ** < 0.005, *** < 0.0005. **** < 0.0001 determined by Student’s t test. Errors bars, SEM
Figure Legend Snippet: Loss of host IFNAR1 increases tumorigenesis and impairs host antitumor immunity. 1 × 105 EO771.LMB cells were injected into the fourth mammary fat pad (IMFP) of wild type (WT) and Ifnar−/− C57BL/6 mice (in which host IFNAR1 is deleted) at day 0 and subsequent alterations to circulating and primary tumor cells assessed. Peripheral blood (PB) was taken at day 7 for FACS analysis and for intracellular staining (ICS) of monocytes was performed at endpoint. Primary tumor a volume (mm3) from WT (n = 4); Ifnar−/− (n = 5) mice and b weights (mg) of WT (n = 7); Ifnar−/− (n = 6) mice at experimental endpoint. Flow cytometric analysis of PB c NK (NK1.1+) cell and d CD69+ NK cell frequency (%); WT (n = 7); Ifnar−/− (n = 6) e Absolute number (cell #) of primary tumor NK cells (n = 5/group). Flow cytometric analysis of primary tumor (n = 5/group) f CD69+ and g IFNγ+ NK cell frequency (%) (h representative flow cytometry plots shown), i NK cell IFNAR1 expression and j mCherry+ EO771.LMB Rae-1 expression, represented as MFI (mean fluorescence intensity). Flow cytometric analysis of primary tumor (n = 5/group) k. CD4+ T cells IFNAR1 expression, l CD4+ IFNγ+ T cells, m CD8+ T cells IFNAR1 expression and n CD8+ IFNγ+ T cells, represented as frequency (%). p values * < 0.05, ** < 0.005, *** < 0.0005. **** < 0.0001 determined by Student’s t test. Errors bars, SEM

Techniques Used: Injection, Staining, Flow Cytometry, Expressing, Fluorescence

Loss of NK cell IFNAR1 impairs NK cell function, may impact adaptive immune regulation of tumorigenesis and increases lung metastasis. 1 × 105 EO771.LMB cells were injected into the fourth mammary fat pad (IMFP) of controliCre and Ifnar−/−NKp46 C57BL/6 mice at day 0 and subsequent alterations to circulating and primary tumor cells assessed. Peripheral blood (PB) was taken at day 7 for FACS analysis and for intracellular staining (ICS) of monocytes was performed at endpoint. a Primary tumor weights (mg) of control (n = 7) and Ifnar−/−NKp46 mice (n = 7) mice at experimental endpoint. Flow cytometric analysis of b absolute number (cell #) of primary tumor NK cells (n = 6/group). c PB CD69+ NK (NK1.1+) cell frequency (%). Primary tumor d CD69+ (e. representative plots shown) and f IFNγ+ NK cell frequency (%) and g IFNAR1 expression, represented as MFI (n = 5/group). Flow cytometric analysis of h CD8+ T cell IFNAR1 (MFI; n = 5/group) and i. PB CD69+ CD8+ T cells, j primary tumor CD69+ CD8+ T cells, k CD8+ IFNγ+ T cells, l. PB CD69+ CD4+ T cells and m primary tumor CD4+ IFNγ+ T cells, expressed as frequency (%). n RT-qPCR of mCherry (EO771.LMB) DNA expression in the lungs post-intravenous (IV) injection of EO771.LMB cells into WT (n = 9), controliCre (n = 5) and Ifnar−/−NKp46 (n = 8) mice at day 24. Representative fluorescence imaging of mCherry (EO771.LMB) in lungs shown for each group. All PB analysis (n = 7/group) and primary tumor analysis (n = 6/group). p values * < 0.05, ** < 0.005, *** < 0.0005. **** < 0.0001 determined by Student’s t test. Errors bars, SEM
Figure Legend Snippet: Loss of NK cell IFNAR1 impairs NK cell function, may impact adaptive immune regulation of tumorigenesis and increases lung metastasis. 1 × 105 EO771.LMB cells were injected into the fourth mammary fat pad (IMFP) of controliCre and Ifnar−/−NKp46 C57BL/6 mice at day 0 and subsequent alterations to circulating and primary tumor cells assessed. Peripheral blood (PB) was taken at day 7 for FACS analysis and for intracellular staining (ICS) of monocytes was performed at endpoint. a Primary tumor weights (mg) of control (n = 7) and Ifnar−/−NKp46 mice (n = 7) mice at experimental endpoint. Flow cytometric analysis of b absolute number (cell #) of primary tumor NK cells (n = 6/group). c PB CD69+ NK (NK1.1+) cell frequency (%). Primary tumor d CD69+ (e. representative plots shown) and f IFNγ+ NK cell frequency (%) and g IFNAR1 expression, represented as MFI (n = 5/group). Flow cytometric analysis of h CD8+ T cell IFNAR1 (MFI; n = 5/group) and i. PB CD69+ CD8+ T cells, j primary tumor CD69+ CD8+ T cells, k CD8+ IFNγ+ T cells, l. PB CD69+ CD4+ T cells and m primary tumor CD4+ IFNγ+ T cells, expressed as frequency (%). n RT-qPCR of mCherry (EO771.LMB) DNA expression in the lungs post-intravenous (IV) injection of EO771.LMB cells into WT (n = 9), controliCre (n = 5) and Ifnar−/−NKp46 (n = 8) mice at day 24. Representative fluorescence imaging of mCherry (EO771.LMB) in lungs shown for each group. All PB analysis (n = 7/group) and primary tumor analysis (n = 6/group). p values * < 0.05, ** < 0.005, *** < 0.0005. **** < 0.0001 determined by Student’s t test. Errors bars, SEM

Techniques Used: Cell Function Assay, Injection, Staining, Expressing, Quantitative RT-PCR, IV Injection, Fluorescence, Imaging



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Loss of host IFNAR1 increases tumorigenesis and impairs host antitumor immunity. 1 × 105 EO771.LMB cells were injected into the fourth mammary fat pad (IMFP) of wild type (WT) and <t>Ifnar−/−</t> C57BL/6 mice (in which host IFNAR1 is deleted) at day 0 and subsequent alterations to circulating and primary tumor cells assessed. Peripheral blood (PB) was taken at day 7 for FACS analysis and for intracellular staining (ICS) of monocytes was performed at endpoint. Primary tumor a volume (mm3) from WT (n = 4); Ifnar−/− (n = 5) mice and b weights (mg) of WT (n = 7); Ifnar−/− (n = 6) mice at experimental endpoint. Flow cytometric analysis of PB c NK (NK1.1+) cell and d CD69+ NK cell frequency (%); WT (n = 7); Ifnar−/− (n = 6) e Absolute number (cell #) of primary tumor NK cells (n = 5/group). Flow cytometric analysis of primary tumor (n = 5/group) f CD69+ and g IFNγ+ NK cell frequency (%) (h representative flow cytometry plots shown), i NK cell IFNAR1 expression and j mCherry+ EO771.LMB Rae-1 expression, represented as MFI (mean fluorescence intensity). Flow cytometric analysis of primary tumor (n = 5/group) k. CD4+ T cells IFNAR1 expression, l CD4+ IFNγ+ T cells, m CD8+ T cells IFNAR1 expression and n CD8+ IFNγ+ T cells, represented as frequency (%). p values * < 0.05, ** < 0.005, *** < 0.0005. **** < 0.0001 determined by Student’s t test. Errors bars, SEM
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Loss of host IFNAR1 increases tumorigenesis and impairs host antitumor immunity. 1 × 105 EO771.LMB cells were injected into the fourth mammary fat pad (IMFP) of wild type (WT) and Ifnar−/− C57BL/6 mice (in which host IFNAR1 is deleted) at day 0 and subsequent alterations to circulating and primary tumor cells assessed. Peripheral blood (PB) was taken at day 7 for FACS analysis and for intracellular staining (ICS) of monocytes was performed at endpoint. Primary tumor a volume (mm3) from WT (n = 4); Ifnar−/− (n = 5) mice and b weights (mg) of WT (n = 7); Ifnar−/− (n = 6) mice at experimental endpoint. Flow cytometric analysis of PB c NK (NK1.1+) cell and d CD69+ NK cell frequency (%); WT (n = 7); Ifnar−/− (n = 6) e Absolute number (cell #) of primary tumor NK cells (n = 5/group). Flow cytometric analysis of primary tumor (n = 5/group) f CD69+ and g IFNγ+ NK cell frequency (%) (h representative flow cytometry plots shown), i NK cell IFNAR1 expression and j mCherry+ EO771.LMB Rae-1 expression, represented as MFI (mean fluorescence intensity). Flow cytometric analysis of primary tumor (n = 5/group) k. CD4+ T cells IFNAR1 expression, l CD4+ IFNγ+ T cells, m CD8+ T cells IFNAR1 expression and n CD8+ IFNγ+ T cells, represented as frequency (%). p values * < 0.05, ** < 0.005, *** < 0.0005. **** < 0.0001 determined by Student’s t test. Errors bars, SEM

Journal: Cancer Immunology, Immunotherapy : CII

Article Title: Loss of type I IFN responsiveness impairs natural killer cell antitumor activity in breast cancer

doi: 10.1007/s00262-021-02857-z

Figure Lengend Snippet: Loss of host IFNAR1 increases tumorigenesis and impairs host antitumor immunity. 1 × 105 EO771.LMB cells were injected into the fourth mammary fat pad (IMFP) of wild type (WT) and Ifnar−/− C57BL/6 mice (in which host IFNAR1 is deleted) at day 0 and subsequent alterations to circulating and primary tumor cells assessed. Peripheral blood (PB) was taken at day 7 for FACS analysis and for intracellular staining (ICS) of monocytes was performed at endpoint. Primary tumor a volume (mm3) from WT (n = 4); Ifnar−/− (n = 5) mice and b weights (mg) of WT (n = 7); Ifnar−/− (n = 6) mice at experimental endpoint. Flow cytometric analysis of PB c NK (NK1.1+) cell and d CD69+ NK cell frequency (%); WT (n = 7); Ifnar−/− (n = 6) e Absolute number (cell #) of primary tumor NK cells (n = 5/group). Flow cytometric analysis of primary tumor (n = 5/group) f CD69+ and g IFNγ+ NK cell frequency (%) (h representative flow cytometry plots shown), i NK cell IFNAR1 expression and j mCherry+ EO771.LMB Rae-1 expression, represented as MFI (mean fluorescence intensity). Flow cytometric analysis of primary tumor (n = 5/group) k. CD4+ T cells IFNAR1 expression, l CD4+ IFNγ+ T cells, m CD8+ T cells IFNAR1 expression and n CD8+ IFNγ+ T cells, represented as frequency (%). p values * < 0.05, ** < 0.005, *** < 0.0005. **** < 0.0001 determined by Student’s t test. Errors bars, SEM

Article Snippet: Cells were stained with panels of antibodies: IFNAR-CD8α-PE-Cy7 (53–6.7), CD4-APC-Cy7 (GK1.5), CD69-APC (H1.2F3), NK1.1-BV421 (PK136), TCR-β-FITC (H57-597), IFN-γ-PE (XMG 1.1) all from BD Biosciences; IgG2a-APC/PE/PE-Cy7 (eBM2a), IgG2a-FITC (eB149/10H5), CD27- PE-Cy7 (LG.7F9), NKG2D-PE-Cy7 (CX5), CD107a-PE (eBio1D4B), CD11b-FITC (M1/70) all from eBioscience.

Techniques: Injection, Staining, Flow Cytometry, Expressing, Fluorescence

Loss of NK cell IFNAR1 impairs NK cell function, may impact adaptive immune regulation of tumorigenesis and increases lung metastasis. 1 × 105 EO771.LMB cells were injected into the fourth mammary fat pad (IMFP) of controliCre and Ifnar−/−NKp46 C57BL/6 mice at day 0 and subsequent alterations to circulating and primary tumor cells assessed. Peripheral blood (PB) was taken at day 7 for FACS analysis and for intracellular staining (ICS) of monocytes was performed at endpoint. a Primary tumor weights (mg) of control (n = 7) and Ifnar−/−NKp46 mice (n = 7) mice at experimental endpoint. Flow cytometric analysis of b absolute number (cell #) of primary tumor NK cells (n = 6/group). c PB CD69+ NK (NK1.1+) cell frequency (%). Primary tumor d CD69+ (e. representative plots shown) and f IFNγ+ NK cell frequency (%) and g IFNAR1 expression, represented as MFI (n = 5/group). Flow cytometric analysis of h CD8+ T cell IFNAR1 (MFI; n = 5/group) and i. PB CD69+ CD8+ T cells, j primary tumor CD69+ CD8+ T cells, k CD8+ IFNγ+ T cells, l. PB CD69+ CD4+ T cells and m primary tumor CD4+ IFNγ+ T cells, expressed as frequency (%). n RT-qPCR of mCherry (EO771.LMB) DNA expression in the lungs post-intravenous (IV) injection of EO771.LMB cells into WT (n = 9), controliCre (n = 5) and Ifnar−/−NKp46 (n = 8) mice at day 24. Representative fluorescence imaging of mCherry (EO771.LMB) in lungs shown for each group. All PB analysis (n = 7/group) and primary tumor analysis (n = 6/group). p values * < 0.05, ** < 0.005, *** < 0.0005. **** < 0.0001 determined by Student’s t test. Errors bars, SEM

Journal: Cancer Immunology, Immunotherapy : CII

Article Title: Loss of type I IFN responsiveness impairs natural killer cell antitumor activity in breast cancer

doi: 10.1007/s00262-021-02857-z

Figure Lengend Snippet: Loss of NK cell IFNAR1 impairs NK cell function, may impact adaptive immune regulation of tumorigenesis and increases lung metastasis. 1 × 105 EO771.LMB cells were injected into the fourth mammary fat pad (IMFP) of controliCre and Ifnar−/−NKp46 C57BL/6 mice at day 0 and subsequent alterations to circulating and primary tumor cells assessed. Peripheral blood (PB) was taken at day 7 for FACS analysis and for intracellular staining (ICS) of monocytes was performed at endpoint. a Primary tumor weights (mg) of control (n = 7) and Ifnar−/−NKp46 mice (n = 7) mice at experimental endpoint. Flow cytometric analysis of b absolute number (cell #) of primary tumor NK cells (n = 6/group). c PB CD69+ NK (NK1.1+) cell frequency (%). Primary tumor d CD69+ (e. representative plots shown) and f IFNγ+ NK cell frequency (%) and g IFNAR1 expression, represented as MFI (n = 5/group). Flow cytometric analysis of h CD8+ T cell IFNAR1 (MFI; n = 5/group) and i. PB CD69+ CD8+ T cells, j primary tumor CD69+ CD8+ T cells, k CD8+ IFNγ+ T cells, l. PB CD69+ CD4+ T cells and m primary tumor CD4+ IFNγ+ T cells, expressed as frequency (%). n RT-qPCR of mCherry (EO771.LMB) DNA expression in the lungs post-intravenous (IV) injection of EO771.LMB cells into WT (n = 9), controliCre (n = 5) and Ifnar−/−NKp46 (n = 8) mice at day 24. Representative fluorescence imaging of mCherry (EO771.LMB) in lungs shown for each group. All PB analysis (n = 7/group) and primary tumor analysis (n = 6/group). p values * < 0.05, ** < 0.005, *** < 0.0005. **** < 0.0001 determined by Student’s t test. Errors bars, SEM

Article Snippet: Cells were stained with panels of antibodies: IFNAR-CD8α-PE-Cy7 (53–6.7), CD4-APC-Cy7 (GK1.5), CD69-APC (H1.2F3), NK1.1-BV421 (PK136), TCR-β-FITC (H57-597), IFN-γ-PE (XMG 1.1) all from BD Biosciences; IgG2a-APC/PE/PE-Cy7 (eBM2a), IgG2a-FITC (eB149/10H5), CD27- PE-Cy7 (LG.7F9), NKG2D-PE-Cy7 (CX5), CD107a-PE (eBio1D4B), CD11b-FITC (M1/70) all from eBioscience.

Techniques: Cell Function Assay, Injection, Staining, Expressing, Quantitative RT-PCR, IV Injection, Fluorescence, Imaging