cd155 plasmid  (Sino Biological)


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    Name:
    CD155 PVR cDNA ORF Clone Mouse untagged
    Description:
    Full length Clone DNA of Mouse poliovirus receptor
    Catalog Number:
    mg50259-ut
    Product Aliases:
    3830421F03Rik cDNA ORF Clone Mouse, CD155 cDNA ORF Clone Mouse, D7Ertd458e cDNA ORF Clone Mouse, HVED cDNA ORF Clone Mouse, mE4 cDNA ORF Clone Mouse, necl-5 cDNA ORF Clone Mouse, PVS cDNA ORF Clone Mouse, Taa1 cDNA ORF Clone Mouse, Tage4 cDNA ORF Clone Mouse
    Price:
    195.0
    Applications:
    Stable or Transient mammalian expression
    Size:
    1Unit
    Category:
    cDNA Clone
    Molecule Name:
    PVR,Tage4,CD155
    Buy from Supplier


    Structured Review

    Sino Biological cd155 plasmid
    CD155 PVR cDNA ORF Clone Mouse untagged
    Full length Clone DNA of Mouse poliovirus receptor
    https://www.bioz.com/result/cd155 plasmid/product/Sino Biological
    Average 91 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    cd155 plasmid - by Bioz Stars, 2021-02
    91/100 stars

    Related Products / Commonly Used Together

    b16f10 - cd155 -- ko
    cd155 plasmid

    Images

    1) Product Images from "CD155 loss enhances tumor suppression via combined host and tumor-intrinsic mechanisms"

    Article Title: CD155 loss enhances tumor suppression via combined host and tumor-intrinsic mechanisms

    Journal: The Journal of Clinical Investigation

    doi: 10.1172/JCI98769

    Tumor-intrinsic CD155 is critical for tumor cell migration and survival. ( A and B ) WT and Rag2 –/– γc –/– mice were injected s.c. with 2 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg2 and sg6) cells ( n = 6/group) ( A ), or 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg2 and sg6) cells ( n = 5–6/group) ( B ), and tumor sizes were measured at the indicated time points (the experiment was performed once). ( C and D ) Rag2 –/– γc –/– mice were injected i.v. with 5 × 10 4 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group) ( C ), or 1 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg6) cells ( n = 6/group) ( D ), and the metastatic burden was quantified in the lungs by counting colonies on the lung surface 14 days after tumor cell inoculation. ( E ) B16F10 control and B16F10- Cd155 –KO (sg6) cells (200 cells/well; n = 3/group) were cultured in 6-well plates for 6 days and stained with crystal violet to assess relative CFU. Images of the colonies of B16F10 control and B16F10- CD155 –KO (sg6) cells are shown, and the relative CFU was assessed (representative of 3 experiments). ( F and G ) B16F10 control or B16F10- CD155 –KO (sg6) cells (1 × 10 5 cells/well) were cultured in 96-well plates. Wounds were made, and wound-healing images were monitored and analyzed, and the percentage of relative wound closure was determined. ( H and I ) B16F10 control and B16F10- CD155 –KO (sg6) cells (1 × 10 5 cells/well) were cultured in 24-well plates under normoxic or hypoxic conditions ( n = 4/group) ( H ) or in media supplemented with 10% or 1% serum ( n = 4/group) ( I ), and apoptosis was evaluated 48 hours later with annexin V and 7-AAD. ( H and I ) Graphs show the representative rate of cell death. * P
    Figure Legend Snippet: Tumor-intrinsic CD155 is critical for tumor cell migration and survival. ( A and B ) WT and Rag2 –/– γc –/– mice were injected s.c. with 2 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg2 and sg6) cells ( n = 6/group) ( A ), or 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg2 and sg6) cells ( n = 5–6/group) ( B ), and tumor sizes were measured at the indicated time points (the experiment was performed once). ( C and D ) Rag2 –/– γc –/– mice were injected i.v. with 5 × 10 4 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group) ( C ), or 1 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg6) cells ( n = 6/group) ( D ), and the metastatic burden was quantified in the lungs by counting colonies on the lung surface 14 days after tumor cell inoculation. ( E ) B16F10 control and B16F10- Cd155 –KO (sg6) cells (200 cells/well; n = 3/group) were cultured in 6-well plates for 6 days and stained with crystal violet to assess relative CFU. Images of the colonies of B16F10 control and B16F10- CD155 –KO (sg6) cells are shown, and the relative CFU was assessed (representative of 3 experiments). ( F and G ) B16F10 control or B16F10- CD155 –KO (sg6) cells (1 × 10 5 cells/well) were cultured in 96-well plates. Wounds were made, and wound-healing images were monitored and analyzed, and the percentage of relative wound closure was determined. ( H and I ) B16F10 control and B16F10- CD155 –KO (sg6) cells (1 × 10 5 cells/well) were cultured in 24-well plates under normoxic or hypoxic conditions ( n = 4/group) ( H ) or in media supplemented with 10% or 1% serum ( n = 4/group) ( I ), and apoptosis was evaluated 48 hours later with annexin V and 7-AAD. ( H and I ) Graphs show the representative rate of cell death. * P

    Techniques Used: Migration, Mouse Assay, Injection, Cell Culture, Staining

    Blockade of PD-1 pathway combined with CD155 deletion enhances tumor growth suppression. ( A ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 6 MCA1956 cells ( n = 10/group). cIg or anti–PD-1 mAb (50 μg) was injected on days 8, 12, 16, and 20, relative to tumor inoculation. ( B ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 MC38 cells ( n = 5–6/group). cIg or anti-PD1 mAb (250 μg) was injected on days 8, 12, 16, and 20, relative to tumor inoculation. ( C ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group). Mice were injected with 250 μg cIg or anti–PD-1/CTLA4 mAb on days 12, 15, 18, and 21, relative to tumor inoculation. ( D ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group). cIg or anti–PD-1 and anti-CTLA4 mAbs (250 μg) were injected into WT mice with B16F10 control cells on days 8, 10, 12, and 14; WT mice with B16F10- Cd155 –KO (sg6) cells on days 12, 14, 16, and 18; Cd155 –/– mice with B16F10 control cells into on days 13, 15, 17, and 19; Cd155 –/– mice with B16F10- Cd155 –KO (sg6) cells on days 17, 19, 21, and 23, relative to tumor inoculation. ( E ) WT mice were injected s.c. with 1 × 10 5 B16F10 control (left) or B16F10- Cd155 –KO (sg6) (right) cells ( n = 5/group). A dose of 250 μg cIg, anti–PD-1 or anti-TIGIT and anti-CD96, or a combination of these mAbs was injected i.p. into WT mice with B16F10 control tumors on days 8, 10, 12, and 14 and into mice with B16F10- Cd155 –KO (sg6) tumors on days 10, 12, 14, and 16, relative to tumor inoculation. ( A – E ) Tumor sizes were measured at the indicated time points. ** P
    Figure Legend Snippet: Blockade of PD-1 pathway combined with CD155 deletion enhances tumor growth suppression. ( A ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 6 MCA1956 cells ( n = 10/group). cIg or anti–PD-1 mAb (50 μg) was injected on days 8, 12, 16, and 20, relative to tumor inoculation. ( B ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 MC38 cells ( n = 5–6/group). cIg or anti-PD1 mAb (250 μg) was injected on days 8, 12, 16, and 20, relative to tumor inoculation. ( C ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group). Mice were injected with 250 μg cIg or anti–PD-1/CTLA4 mAb on days 12, 15, 18, and 21, relative to tumor inoculation. ( D ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group). cIg or anti–PD-1 and anti-CTLA4 mAbs (250 μg) were injected into WT mice with B16F10 control cells on days 8, 10, 12, and 14; WT mice with B16F10- Cd155 –KO (sg6) cells on days 12, 14, 16, and 18; Cd155 –/– mice with B16F10 control cells into on days 13, 15, 17, and 19; Cd155 –/– mice with B16F10- Cd155 –KO (sg6) cells on days 17, 19, 21, and 23, relative to tumor inoculation. ( E ) WT mice were injected s.c. with 1 × 10 5 B16F10 control (left) or B16F10- Cd155 –KO (sg6) (right) cells ( n = 5/group). A dose of 250 μg cIg, anti–PD-1 or anti-TIGIT and anti-CD96, or a combination of these mAbs was injected i.p. into WT mice with B16F10 control tumors on days 8, 10, 12, and 14 and into mice with B16F10- Cd155 –KO (sg6) tumors on days 10, 12, 14, and 16, relative to tumor inoculation. ( A – E ) Tumor sizes were measured at the indicated time points. ** P

    Techniques Used: Mouse Assay, Injection

    Tumor growth and metastasis are inhibited in Cd155 –/– mice in a BM cell–dependent manner. ( A – C ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 cells ( n = 6–7/group) ( A ) or 5 × 10 5 SM1WT1 cells ( n = 7/group) ( B ), or 5 × 10 5 MC38 cells ( n = 5–6/group) ( C ), and tumor sizes were measured at the indicated time points. ( D and E ) WT and Cd155 –/– mice were challenged i.v. with 2 × 10 5 B16F10 cells ( n = 8–11/group) ( D ) or 7.5 × 10 5 LWT1 cells ( n = 6–7/group) ( E ), 2 weeks after tumor inoculation, and metastatic burden was quantified in the lungs by counting colonies on the lung surface. ( F and G ) WT and Cd155 –/– mice were treated with 100 μg cIg, or 100 μg anti-CD8β (53.5.8, CD8 + T cell depletion), or 100 μg anti-CD4 (GK1.5, CD4 + T cell depletion) plus 100 μg anti-CD8β (53.5.8), or 50 μg anti-asGM1 (NK cell depletion) on days –1, 0, 7, and 14 for tumor growth, or on days –1, 0, and 7 for tumor metastasis relative to tumor inoculation. Mice were challenged s.c. with 1 × 10 5 B16F10 cells ( n = 5–6/group; the experiment was performed once) ( F ), and tumor sizes were measured at the indicated time points, or mice were challenged i.v. with 7.5 × 10 5 LWT1 cells ( n = 6/group) ( G ), and lung metastases were quantified 2 weeks after tumor inoculation. ( H and J ) Ptprc a (CD45.1 + ) and Cd155 –/– (CD45.2 + ) mice were irradiated twice (total radiation dose: 1,050 cGy/rad), and 5 × 10 6 BM cells from Ptprc a or Cd155 –/– mice were then i.v. injected into each irradiated mouse to construct BM chimeric mice ( H ). Mice were then challenged s.c. with 1 × 10 5 B16F10 ( I ) or i.v. with 2 × 10 5 B16F10 ( J ) cells, respectively ( n = 10/group; the experiment was performed once for both I and J ). Tumor sizes were measured at the indicated time points ( I ), and lung metastases were quantified 2 weeks after tumor inoculation ( J ). * P
    Figure Legend Snippet: Tumor growth and metastasis are inhibited in Cd155 –/– mice in a BM cell–dependent manner. ( A – C ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 cells ( n = 6–7/group) ( A ) or 5 × 10 5 SM1WT1 cells ( n = 7/group) ( B ), or 5 × 10 5 MC38 cells ( n = 5–6/group) ( C ), and tumor sizes were measured at the indicated time points. ( D and E ) WT and Cd155 –/– mice were challenged i.v. with 2 × 10 5 B16F10 cells ( n = 8–11/group) ( D ) or 7.5 × 10 5 LWT1 cells ( n = 6–7/group) ( E ), 2 weeks after tumor inoculation, and metastatic burden was quantified in the lungs by counting colonies on the lung surface. ( F and G ) WT and Cd155 –/– mice were treated with 100 μg cIg, or 100 μg anti-CD8β (53.5.8, CD8 + T cell depletion), or 100 μg anti-CD4 (GK1.5, CD4 + T cell depletion) plus 100 μg anti-CD8β (53.5.8), or 50 μg anti-asGM1 (NK cell depletion) on days –1, 0, 7, and 14 for tumor growth, or on days –1, 0, and 7 for tumor metastasis relative to tumor inoculation. Mice were challenged s.c. with 1 × 10 5 B16F10 cells ( n = 5–6/group; the experiment was performed once) ( F ), and tumor sizes were measured at the indicated time points, or mice were challenged i.v. with 7.5 × 10 5 LWT1 cells ( n = 6/group) ( G ), and lung metastases were quantified 2 weeks after tumor inoculation. ( H and J ) Ptprc a (CD45.1 + ) and Cd155 –/– (CD45.2 + ) mice were irradiated twice (total radiation dose: 1,050 cGy/rad), and 5 × 10 6 BM cells from Ptprc a or Cd155 –/– mice were then i.v. injected into each irradiated mouse to construct BM chimeric mice ( H ). Mice were then challenged s.c. with 1 × 10 5 B16F10 ( I ) or i.v. with 2 × 10 5 B16F10 ( J ) cells, respectively ( n = 10/group; the experiment was performed once for both I and J ). Tumor sizes were measured at the indicated time points ( I ), and lung metastases were quantified 2 weeks after tumor inoculation ( J ). * P

    Techniques Used: Mouse Assay, Injection, Irradiation, Construct

    Inhibition of tumor growth and metastasis in Cd155 –/– mice is DNAM-1 dependent. ( A ) DNAM-1, CD96, and TIGIT expression was analyzed on day 12 on tumor-infiltrating CD4 + T cells, CD8 + T cells, and NK cells after inoculation of 1 × 10 5 B16F10 cells in WT and CD155 –/– mice ( n = 5/group). The mean fluorescence intensity (MFI) is shown. ( B ) Tumor sizes were measured at the indicated time points for WT and Cd155 –/– mice ( n = 5–6/group) treated with 100 μg cIg, 100 μg anti-CD8β (clone 53.5.8), 250 μg anti-DNAM-1 (clone 480.1), or 50 μg anti-asGM1 on days –1, 0, 7, and 14, relative to inoculation of 1 × 10 5 B16F10 cells (the experiment was performed twice). ( C ) Splenocytes from naive C57BL/6 WT and Cd155 –/– mice ( n = 3) were stimulated with 1 μg/ml anti-CD3 and 2 μg/ml anti-CD28 for 24 hours, and the expression of IFN-γ on CD8 + T cells was analyzed by flow cytometry (data are representative of 2 experiments). ( D ) WT and Cd155 –/– mice ( n = 5/group) were injected i.v. with 1 × 10 5 B16F10 melanoma cells and treated on days –1, 0, and 7, relative to tumor inoculation with 250 μg cIg (clone 1-1), 250 μg anti–DNAM-1 (clone 480.1), or 50 μg anti-asGM1. Metastatic burden was quantified in the lungs by counting colonies on the lung surface 14 days after tumor cell inoculation ( n = 5/group; the experiment was performed once). ( E ) NK cells from the spleens of naive C57BL/6 WT and Cd155 –/– mice ( n = 4) were purified and stimulated with the indicated concentrations of IL-12 and IL-18 for 24 hours, and the expression of IFN-γ on NK cells was analyzed by flow cytometry. * P
    Figure Legend Snippet: Inhibition of tumor growth and metastasis in Cd155 –/– mice is DNAM-1 dependent. ( A ) DNAM-1, CD96, and TIGIT expression was analyzed on day 12 on tumor-infiltrating CD4 + T cells, CD8 + T cells, and NK cells after inoculation of 1 × 10 5 B16F10 cells in WT and CD155 –/– mice ( n = 5/group). The mean fluorescence intensity (MFI) is shown. ( B ) Tumor sizes were measured at the indicated time points for WT and Cd155 –/– mice ( n = 5–6/group) treated with 100 μg cIg, 100 μg anti-CD8β (clone 53.5.8), 250 μg anti-DNAM-1 (clone 480.1), or 50 μg anti-asGM1 on days –1, 0, 7, and 14, relative to inoculation of 1 × 10 5 B16F10 cells (the experiment was performed twice). ( C ) Splenocytes from naive C57BL/6 WT and Cd155 –/– mice ( n = 3) were stimulated with 1 μg/ml anti-CD3 and 2 μg/ml anti-CD28 for 24 hours, and the expression of IFN-γ on CD8 + T cells was analyzed by flow cytometry (data are representative of 2 experiments). ( D ) WT and Cd155 –/– mice ( n = 5/group) were injected i.v. with 1 × 10 5 B16F10 melanoma cells and treated on days –1, 0, and 7, relative to tumor inoculation with 250 μg cIg (clone 1-1), 250 μg anti–DNAM-1 (clone 480.1), or 50 μg anti-asGM1. Metastatic burden was quantified in the lungs by counting colonies on the lung surface 14 days after tumor cell inoculation ( n = 5/group; the experiment was performed once). ( E ) NK cells from the spleens of naive C57BL/6 WT and Cd155 –/– mice ( n = 4) were purified and stimulated with the indicated concentrations of IL-12 and IL-18 for 24 hours, and the expression of IFN-γ on NK cells was analyzed by flow cytometry. * P

    Techniques Used: Inhibition, Mouse Assay, Expressing, Fluorescence, Flow Cytometry, Cytometry, Injection, Purification

    Deletion of tumor CD155 decreases tumor growth and metastasis. ( A – D ) WT mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg2 and sg6) cells ( n = 6/group) ( A ); 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg2 and sg6) cells ( n = 5–6/group) ( B ); 5 × 10 5 MC38 control or MC38- Cd155 –KO (sg2 and sg6) cells ( n = 5/group) ( C ); or 1 × 10 6 MCA1956 control or MCA1956- Cd155 –KO (sg6) cells ( n = 5/group) ( D ), and tumor sizes were measured at the indicated time points. ( E – G ) WT mice were injected i.v. with 2 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5–6/group) ( E ); 7.5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg2 and sg6) cells ( n = 4–7/group) ( F ); or 2 × 10 5 MC38 control or MC38- Cd155 –KO (sg2 and sg6) cells ( n = 7/group) ( G ). Metastatic burden in the lungs was quantified by counting colonies on the lung surface 14 days after tumor inoculation. ( H and I ) Female BALB/c WT mice were injected into the mammary fat pad with 5 × 10 4 4T1.2 control or 4T1.2- Cd155 –KO cells, and tumors were resected on day 14. In 1 group, the metastatic burden was quantified in the lungs by counting colonies on the lung surface on day 30 ( n = 9/group) ( H ), and in another group, the survival was monitored ( I ) ( n = 14–20/group; experiment was performed twice). * P
    Figure Legend Snippet: Deletion of tumor CD155 decreases tumor growth and metastasis. ( A – D ) WT mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg2 and sg6) cells ( n = 6/group) ( A ); 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg2 and sg6) cells ( n = 5–6/group) ( B ); 5 × 10 5 MC38 control or MC38- Cd155 –KO (sg2 and sg6) cells ( n = 5/group) ( C ); or 1 × 10 6 MCA1956 control or MCA1956- Cd155 –KO (sg6) cells ( n = 5/group) ( D ), and tumor sizes were measured at the indicated time points. ( E – G ) WT mice were injected i.v. with 2 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5–6/group) ( E ); 7.5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg2 and sg6) cells ( n = 4–7/group) ( F ); or 2 × 10 5 MC38 control or MC38- Cd155 –KO (sg2 and sg6) cells ( n = 7/group) ( G ). Metastatic burden in the lungs was quantified by counting colonies on the lung surface 14 days after tumor inoculation. ( H and I ) Female BALB/c WT mice were injected into the mammary fat pad with 5 × 10 4 4T1.2 control or 4T1.2- Cd155 –KO cells, and tumors were resected on day 14. In 1 group, the metastatic burden was quantified in the lungs by counting colonies on the lung surface on day 30 ( n = 9/group) ( H ), and in another group, the survival was monitored ( I ) ( n = 14–20/group; experiment was performed twice). * P

    Techniques Used: Mouse Assay, Injection

    Deletion of CD155 from host and tumor enhances the suppression of tumor progression. ( A ) Experimental protocol for the induction of primary s.c. or lung metastases with control or Cd155 -KO (sg2 and/or sg6) tumor cells in WT or Cd155 –/– mice. ( B ) WT and Cd155 –/– mice were injected i.v. with 1 × 10 5 B16F10 control, B16F10- Cd155 –KO (sg2), or B16F10- Cd155 –KO (sg6) cells ( n = 5–6/group). Metastatic burden was quantified in the lungs by counting colonies on the lung surface 14 days after tumor cell inoculation (the experiment was performed once). ( C ) WT and Cd155 –/– mice were injected i.v. with 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg6) cells ( n = 7–10/group). Fourteen days after tumor inoculation, the metastatic burden was quantified in the lungs by counting colonies on the lung surface (the experiment was performed once). ( D – F ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group) ( D ); 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg6) cells ( n = 8–9/group) ( E ); or 5 × 10 5 MC38 control or MC38- Cd155 –KO (sg6) cells ( n = 5/group) ( F ), and tumor sizes were measured at the indicated time points. ( G ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group). A dose of 250 μg cIg (clone 1-1) or anti–DNAM-1 (clone 480.1) mAb was injected on days –1, 0, and 7, relative to tumor inoculation (experiment was performed once). * P
    Figure Legend Snippet: Deletion of CD155 from host and tumor enhances the suppression of tumor progression. ( A ) Experimental protocol for the induction of primary s.c. or lung metastases with control or Cd155 -KO (sg2 and/or sg6) tumor cells in WT or Cd155 –/– mice. ( B ) WT and Cd155 –/– mice were injected i.v. with 1 × 10 5 B16F10 control, B16F10- Cd155 –KO (sg2), or B16F10- Cd155 –KO (sg6) cells ( n = 5–6/group). Metastatic burden was quantified in the lungs by counting colonies on the lung surface 14 days after tumor cell inoculation (the experiment was performed once). ( C ) WT and Cd155 –/– mice were injected i.v. with 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg6) cells ( n = 7–10/group). Fourteen days after tumor inoculation, the metastatic burden was quantified in the lungs by counting colonies on the lung surface (the experiment was performed once). ( D – F ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group) ( D ); 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg6) cells ( n = 8–9/group) ( E ); or 5 × 10 5 MC38 control or MC38- Cd155 –KO (sg6) cells ( n = 5/group) ( F ), and tumor sizes were measured at the indicated time points. ( G ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group). A dose of 250 μg cIg (clone 1-1) or anti–DNAM-1 (clone 480.1) mAb was injected on days –1, 0, and 7, relative to tumor inoculation (experiment was performed once). * P

    Techniques Used: Mouse Assay, Injection

    CD155 is expressed in malignant cells and tumor-infiltrating myeloid cells in human and mouse tumors. ( A and B ) Representative multiplexed IHC images of human primary cutaneous melanoma samples. CD155 (green) was distributed broadly within the carcinoma element of human melanoma, identified by HMB45 positivity (orange). Tumor-infiltrating myeloid cells were revealed by CD14 (red) or CD11c (yellow) positivity. The dotted line circumscribes HMB45 + tumor cells in a representative human melanoma TMA core. The merged image shows high colocalization of CD155 and HMB45. Scale bars: 200 μm ( A ) and 50 μm ( B ). ( C ) Colocalization of CD155 in tumor-infiltrating myeloid cells in human melanoma. CD11c (yellow) and CD14 (red) discriminated different populations of tumor-infiltrating cells, including CD11c + CD14 – DCs (yellow arrows), CD11c + CD14 + myeloid cells (white arrows), and CD11c – CD14 + monocytes/macrophages (red arrows). CD155 staining (green) was colocalized within each of these myeloid populations, as indicated in the merged panel. Scale bar: 50 μm. ( A – C ) Nuclei were stained with DAPI (blue) in each panel. ( D and E ) WT mice were injected s.c. with 1 × 10 5 B16F10 cells ( n = 5/group), and tumor samples were digested and analyzed on day 12. Tumor cells were gated by FSC hi SSC hi Zombie-yellow – CD45.2 – expression. ( D ) CD155 and PD-L1 expression on ex vivo B16F10 tumor cells is shown. ( E ) CD11b + CD11c + and CD11b + CD11c – tumor-infiltrating myeloid cell populations were gated by FSC lo SSC lo Zombie-yellow – CD45.2 + .
    Figure Legend Snippet: CD155 is expressed in malignant cells and tumor-infiltrating myeloid cells in human and mouse tumors. ( A and B ) Representative multiplexed IHC images of human primary cutaneous melanoma samples. CD155 (green) was distributed broadly within the carcinoma element of human melanoma, identified by HMB45 positivity (orange). Tumor-infiltrating myeloid cells were revealed by CD14 (red) or CD11c (yellow) positivity. The dotted line circumscribes HMB45 + tumor cells in a representative human melanoma TMA core. The merged image shows high colocalization of CD155 and HMB45. Scale bars: 200 μm ( A ) and 50 μm ( B ). ( C ) Colocalization of CD155 in tumor-infiltrating myeloid cells in human melanoma. CD11c (yellow) and CD14 (red) discriminated different populations of tumor-infiltrating cells, including CD11c + CD14 – DCs (yellow arrows), CD11c + CD14 + myeloid cells (white arrows), and CD11c – CD14 + monocytes/macrophages (red arrows). CD155 staining (green) was colocalized within each of these myeloid populations, as indicated in the merged panel. Scale bar: 50 μm. ( A – C ) Nuclei were stained with DAPI (blue) in each panel. ( D and E ) WT mice were injected s.c. with 1 × 10 5 B16F10 cells ( n = 5/group), and tumor samples were digested and analyzed on day 12. Tumor cells were gated by FSC hi SSC hi Zombie-yellow – CD45.2 – expression. ( D ) CD155 and PD-L1 expression on ex vivo B16F10 tumor cells is shown. ( E ) CD11b + CD11c + and CD11b + CD11c – tumor-infiltrating myeloid cell populations were gated by FSC lo SSC lo Zombie-yellow – CD45.2 + .

    Techniques Used: Immunohistochemistry, Staining, Mouse Assay, Injection, Expressing, Ex Vivo

    2) Product Images from "CD155 loss enhances tumor suppression via combined host and tumor-intrinsic mechanisms"

    Article Title: CD155 loss enhances tumor suppression via combined host and tumor-intrinsic mechanisms

    Journal: The Journal of Clinical Investigation

    doi: 10.1172/JCI98769

    Tumor-intrinsic CD155 is critical for tumor cell migration and survival. ( A and B ) WT and Rag2 –/– γc –/– mice were injected s.c. with 2 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg2 and sg6) cells ( n = 6/group) ( A ), or 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg2 and sg6) cells ( n = 5–6/group) ( B ), and tumor sizes were measured at the indicated time points (the experiment was performed once). ( C and D ) Rag2 –/– γc –/– mice were injected i.v. with 5 × 10 4 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group) ( C ), or 1 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg6) cells ( n = 6/group) ( D ), and the metastatic burden was quantified in the lungs by counting colonies on the lung surface 14 days after tumor cell inoculation. ( E ) B16F10 control and B16F10- Cd155 –KO (sg6) cells (200 cells/well; n = 3/group) were cultured in 6-well plates for 6 days and stained with crystal violet to assess relative CFU. Images of the colonies of B16F10 control and B16F10- CD155 –KO (sg6) cells are shown, and the relative CFU was assessed (representative of 3 experiments). ( F and G ) B16F10 control or B16F10- CD155 –KO (sg6) cells (1 × 10 5 cells/well) were cultured in 96-well plates. Wounds were made, and wound-healing images were monitored and analyzed, and the percentage of relative wound closure was determined. ( H and I ) B16F10 control and B16F10- CD155 –KO (sg6) cells (1 × 10 5 cells/well) were cultured in 24-well plates under normoxic or hypoxic conditions ( n = 4/group) ( H ) or in media supplemented with 10% or 1% serum ( n = 4/group) ( I ), and apoptosis was evaluated 48 hours later with annexin V and 7-AAD. ( H and I ) Graphs show the representative rate of cell death. * P
    Figure Legend Snippet: Tumor-intrinsic CD155 is critical for tumor cell migration and survival. ( A and B ) WT and Rag2 –/– γc –/– mice were injected s.c. with 2 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg2 and sg6) cells ( n = 6/group) ( A ), or 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg2 and sg6) cells ( n = 5–6/group) ( B ), and tumor sizes were measured at the indicated time points (the experiment was performed once). ( C and D ) Rag2 –/– γc –/– mice were injected i.v. with 5 × 10 4 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group) ( C ), or 1 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg6) cells ( n = 6/group) ( D ), and the metastatic burden was quantified in the lungs by counting colonies on the lung surface 14 days after tumor cell inoculation. ( E ) B16F10 control and B16F10- Cd155 –KO (sg6) cells (200 cells/well; n = 3/group) were cultured in 6-well plates for 6 days and stained with crystal violet to assess relative CFU. Images of the colonies of B16F10 control and B16F10- CD155 –KO (sg6) cells are shown, and the relative CFU was assessed (representative of 3 experiments). ( F and G ) B16F10 control or B16F10- CD155 –KO (sg6) cells (1 × 10 5 cells/well) were cultured in 96-well plates. Wounds were made, and wound-healing images were monitored and analyzed, and the percentage of relative wound closure was determined. ( H and I ) B16F10 control and B16F10- CD155 –KO (sg6) cells (1 × 10 5 cells/well) were cultured in 24-well plates under normoxic or hypoxic conditions ( n = 4/group) ( H ) or in media supplemented with 10% or 1% serum ( n = 4/group) ( I ), and apoptosis was evaluated 48 hours later with annexin V and 7-AAD. ( H and I ) Graphs show the representative rate of cell death. * P

    Techniques Used: Migration, Mouse Assay, Injection, Cell Culture, Staining

    Blockade of PD-1 pathway combined with CD155 deletion enhances tumor growth suppression. ( A ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 6 MCA1956 cells ( n = 10/group). cIg or anti–PD-1 mAb (50 μg) was injected on days 8, 12, 16, and 20, relative to tumor inoculation. ( B ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 MC38 cells ( n = 5–6/group). cIg or anti-PD1 mAb (250 μg) was injected on days 8, 12, 16, and 20, relative to tumor inoculation. ( C ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group). Mice were injected with 250 μg cIg or anti–PD-1/CTLA4 mAb on days 12, 15, 18, and 21, relative to tumor inoculation. ( D ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group). cIg or anti–PD-1 and anti-CTLA4 mAbs (250 μg) were injected into WT mice with B16F10 control cells on days 8, 10, 12, and 14; WT mice with B16F10- Cd155 –KO (sg6) cells on days 12, 14, 16, and 18; Cd155 –/– mice with B16F10 control cells into on days 13, 15, 17, and 19; Cd155 –/– mice with B16F10- Cd155 –KO (sg6) cells on days 17, 19, 21, and 23, relative to tumor inoculation. ( E ) WT mice were injected s.c. with 1 × 10 5 B16F10 control (left) or B16F10- Cd155 –KO (sg6) (right) cells ( n = 5/group). A dose of 250 μg cIg, anti–PD-1 or anti-TIGIT and anti-CD96, or a combination of these mAbs was injected i.p. into WT mice with B16F10 control tumors on days 8, 10, 12, and 14 and into mice with B16F10- Cd155 –KO (sg6) tumors on days 10, 12, 14, and 16, relative to tumor inoculation. ( A – E ) Tumor sizes were measured at the indicated time points. ** P
    Figure Legend Snippet: Blockade of PD-1 pathway combined with CD155 deletion enhances tumor growth suppression. ( A ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 6 MCA1956 cells ( n = 10/group). cIg or anti–PD-1 mAb (50 μg) was injected on days 8, 12, 16, and 20, relative to tumor inoculation. ( B ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 MC38 cells ( n = 5–6/group). cIg or anti-PD1 mAb (250 μg) was injected on days 8, 12, 16, and 20, relative to tumor inoculation. ( C ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group). Mice were injected with 250 μg cIg or anti–PD-1/CTLA4 mAb on days 12, 15, 18, and 21, relative to tumor inoculation. ( D ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group). cIg or anti–PD-1 and anti-CTLA4 mAbs (250 μg) were injected into WT mice with B16F10 control cells on days 8, 10, 12, and 14; WT mice with B16F10- Cd155 –KO (sg6) cells on days 12, 14, 16, and 18; Cd155 –/– mice with B16F10 control cells into on days 13, 15, 17, and 19; Cd155 –/– mice with B16F10- Cd155 –KO (sg6) cells on days 17, 19, 21, and 23, relative to tumor inoculation. ( E ) WT mice were injected s.c. with 1 × 10 5 B16F10 control (left) or B16F10- Cd155 –KO (sg6) (right) cells ( n = 5/group). A dose of 250 μg cIg, anti–PD-1 or anti-TIGIT and anti-CD96, or a combination of these mAbs was injected i.p. into WT mice with B16F10 control tumors on days 8, 10, 12, and 14 and into mice with B16F10- Cd155 –KO (sg6) tumors on days 10, 12, 14, and 16, relative to tumor inoculation. ( A – E ) Tumor sizes were measured at the indicated time points. ** P

    Techniques Used: Mouse Assay, Injection

    Tumor growth and metastasis are inhibited in Cd155 –/– mice in a BM cell–dependent manner. ( A – C ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 cells ( n = 6–7/group) ( A ) or 5 × 10 5 SM1WT1 cells ( n = 7/group) ( B ), or 5 × 10 5 MC38 cells ( n = 5–6/group) ( C ), and tumor sizes were measured at the indicated time points. ( D and E ) WT and Cd155 –/– mice were challenged i.v. with 2 × 10 5 B16F10 cells ( n = 8–11/group) ( D ) or 7.5 × 10 5 LWT1 cells ( n = 6–7/group) ( E ), 2 weeks after tumor inoculation, and metastatic burden was quantified in the lungs by counting colonies on the lung surface. ( F and G ) WT and Cd155 –/– mice were treated with 100 μg cIg, or 100 μg anti-CD8β (53.5.8, CD8 + T cell depletion), or 100 μg anti-CD4 (GK1.5, CD4 + T cell depletion) plus 100 μg anti-CD8β (53.5.8), or 50 μg anti-asGM1 (NK cell depletion) on days –1, 0, 7, and 14 for tumor growth, or on days –1, 0, and 7 for tumor metastasis relative to tumor inoculation. Mice were challenged s.c. with 1 × 10 5 B16F10 cells ( n = 5–6/group; the experiment was performed once) ( F ), and tumor sizes were measured at the indicated time points, or mice were challenged i.v. with 7.5 × 10 5 LWT1 cells ( n = 6/group) ( G ), and lung metastases were quantified 2 weeks after tumor inoculation. ( H and J ) Ptprc a (CD45.1 + ) and Cd155 –/– (CD45.2 + ) mice were irradiated twice (total radiation dose: 1,050 cGy/rad), and 5 × 10 6 BM cells from Ptprc a or Cd155 –/– mice were then i.v. injected into each irradiated mouse to construct BM chimeric mice ( H ). Mice were then challenged s.c. with 1 × 10 5 B16F10 ( I ) or i.v. with 2 × 10 5 B16F10 ( J ) cells, respectively ( n = 10/group; the experiment was performed once for both I and J ). Tumor sizes were measured at the indicated time points ( I ), and lung metastases were quantified 2 weeks after tumor inoculation ( J ). * P
    Figure Legend Snippet: Tumor growth and metastasis are inhibited in Cd155 –/– mice in a BM cell–dependent manner. ( A – C ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 cells ( n = 6–7/group) ( A ) or 5 × 10 5 SM1WT1 cells ( n = 7/group) ( B ), or 5 × 10 5 MC38 cells ( n = 5–6/group) ( C ), and tumor sizes were measured at the indicated time points. ( D and E ) WT and Cd155 –/– mice were challenged i.v. with 2 × 10 5 B16F10 cells ( n = 8–11/group) ( D ) or 7.5 × 10 5 LWT1 cells ( n = 6–7/group) ( E ), 2 weeks after tumor inoculation, and metastatic burden was quantified in the lungs by counting colonies on the lung surface. ( F and G ) WT and Cd155 –/– mice were treated with 100 μg cIg, or 100 μg anti-CD8β (53.5.8, CD8 + T cell depletion), or 100 μg anti-CD4 (GK1.5, CD4 + T cell depletion) plus 100 μg anti-CD8β (53.5.8), or 50 μg anti-asGM1 (NK cell depletion) on days –1, 0, 7, and 14 for tumor growth, or on days –1, 0, and 7 for tumor metastasis relative to tumor inoculation. Mice were challenged s.c. with 1 × 10 5 B16F10 cells ( n = 5–6/group; the experiment was performed once) ( F ), and tumor sizes were measured at the indicated time points, or mice were challenged i.v. with 7.5 × 10 5 LWT1 cells ( n = 6/group) ( G ), and lung metastases were quantified 2 weeks after tumor inoculation. ( H and J ) Ptprc a (CD45.1 + ) and Cd155 –/– (CD45.2 + ) mice were irradiated twice (total radiation dose: 1,050 cGy/rad), and 5 × 10 6 BM cells from Ptprc a or Cd155 –/– mice were then i.v. injected into each irradiated mouse to construct BM chimeric mice ( H ). Mice were then challenged s.c. with 1 × 10 5 B16F10 ( I ) or i.v. with 2 × 10 5 B16F10 ( J ) cells, respectively ( n = 10/group; the experiment was performed once for both I and J ). Tumor sizes were measured at the indicated time points ( I ), and lung metastases were quantified 2 weeks after tumor inoculation ( J ). * P

    Techniques Used: Mouse Assay, Injection, Irradiation, Construct

    Inhibition of tumor growth and metastasis in Cd155 –/– mice is DNAM-1 dependent. ( A ) DNAM-1, CD96, and TIGIT expression was analyzed on day 12 on tumor-infiltrating CD4 + T cells, CD8 + T cells, and NK cells after inoculation of 1 × 10 5 B16F10 cells in WT and CD155 –/– mice ( n = 5/group). The mean fluorescence intensity (MFI) is shown. ( B ) Tumor sizes were measured at the indicated time points for WT and Cd155 –/– mice ( n = 5–6/group) treated with 100 μg cIg, 100 μg anti-CD8β (clone 53.5.8), 250 μg anti-DNAM-1 (clone 480.1), or 50 μg anti-asGM1 on days –1, 0, 7, and 14, relative to inoculation of 1 × 10 5 B16F10 cells (the experiment was performed twice). ( C ) Splenocytes from naive C57BL/6 WT and Cd155 –/– mice ( n = 3) were stimulated with 1 μg/ml anti-CD3 and 2 μg/ml anti-CD28 for 24 hours, and the expression of IFN-γ on CD8 + T cells was analyzed by flow cytometry (data are representative of 2 experiments). ( D ) WT and Cd155 –/– mice ( n = 5/group) were injected i.v. with 1 × 10 5 B16F10 melanoma cells and treated on days –1, 0, and 7, relative to tumor inoculation with 250 μg cIg (clone 1-1), 250 μg anti–DNAM-1 (clone 480.1), or 50 μg anti-asGM1. Metastatic burden was quantified in the lungs by counting colonies on the lung surface 14 days after tumor cell inoculation ( n = 5/group; the experiment was performed once). ( E ) NK cells from the spleens of naive C57BL/6 WT and Cd155 –/– mice ( n = 4) were purified and stimulated with the indicated concentrations of IL-12 and IL-18 for 24 hours, and the expression of IFN-γ on NK cells was analyzed by flow cytometry. * P
    Figure Legend Snippet: Inhibition of tumor growth and metastasis in Cd155 –/– mice is DNAM-1 dependent. ( A ) DNAM-1, CD96, and TIGIT expression was analyzed on day 12 on tumor-infiltrating CD4 + T cells, CD8 + T cells, and NK cells after inoculation of 1 × 10 5 B16F10 cells in WT and CD155 –/– mice ( n = 5/group). The mean fluorescence intensity (MFI) is shown. ( B ) Tumor sizes were measured at the indicated time points for WT and Cd155 –/– mice ( n = 5–6/group) treated with 100 μg cIg, 100 μg anti-CD8β (clone 53.5.8), 250 μg anti-DNAM-1 (clone 480.1), or 50 μg anti-asGM1 on days –1, 0, 7, and 14, relative to inoculation of 1 × 10 5 B16F10 cells (the experiment was performed twice). ( C ) Splenocytes from naive C57BL/6 WT and Cd155 –/– mice ( n = 3) were stimulated with 1 μg/ml anti-CD3 and 2 μg/ml anti-CD28 for 24 hours, and the expression of IFN-γ on CD8 + T cells was analyzed by flow cytometry (data are representative of 2 experiments). ( D ) WT and Cd155 –/– mice ( n = 5/group) were injected i.v. with 1 × 10 5 B16F10 melanoma cells and treated on days –1, 0, and 7, relative to tumor inoculation with 250 μg cIg (clone 1-1), 250 μg anti–DNAM-1 (clone 480.1), or 50 μg anti-asGM1. Metastatic burden was quantified in the lungs by counting colonies on the lung surface 14 days after tumor cell inoculation ( n = 5/group; the experiment was performed once). ( E ) NK cells from the spleens of naive C57BL/6 WT and Cd155 –/– mice ( n = 4) were purified and stimulated with the indicated concentrations of IL-12 and IL-18 for 24 hours, and the expression of IFN-γ on NK cells was analyzed by flow cytometry. * P

    Techniques Used: Inhibition, Mouse Assay, Expressing, Fluorescence, Flow Cytometry, Cytometry, Injection, Purification

    Deletion of tumor CD155 decreases tumor growth and metastasis. ( A – D ) WT mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg2 and sg6) cells ( n = 6/group) ( A ); 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg2 and sg6) cells ( n = 5–6/group) ( B ); 5 × 10 5 MC38 control or MC38- Cd155 –KO (sg2 and sg6) cells ( n = 5/group) ( C ); or 1 × 10 6 MCA1956 control or MCA1956- Cd155 –KO (sg6) cells ( n = 5/group) ( D ), and tumor sizes were measured at the indicated time points. ( E – G ) WT mice were injected i.v. with 2 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5–6/group) ( E ); 7.5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg2 and sg6) cells ( n = 4–7/group) ( F ); or 2 × 10 5 MC38 control or MC38- Cd155 –KO (sg2 and sg6) cells ( n = 7/group) ( G ). Metastatic burden in the lungs was quantified by counting colonies on the lung surface 14 days after tumor inoculation. ( H and I ) Female BALB/c WT mice were injected into the mammary fat pad with 5 × 10 4 4T1.2 control or 4T1.2- Cd155 –KO cells, and tumors were resected on day 14. In 1 group, the metastatic burden was quantified in the lungs by counting colonies on the lung surface on day 30 ( n = 9/group) ( H ), and in another group, the survival was monitored ( I ) ( n = 14–20/group; experiment was performed twice). * P
    Figure Legend Snippet: Deletion of tumor CD155 decreases tumor growth and metastasis. ( A – D ) WT mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg2 and sg6) cells ( n = 6/group) ( A ); 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg2 and sg6) cells ( n = 5–6/group) ( B ); 5 × 10 5 MC38 control or MC38- Cd155 –KO (sg2 and sg6) cells ( n = 5/group) ( C ); or 1 × 10 6 MCA1956 control or MCA1956- Cd155 –KO (sg6) cells ( n = 5/group) ( D ), and tumor sizes were measured at the indicated time points. ( E – G ) WT mice were injected i.v. with 2 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5–6/group) ( E ); 7.5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg2 and sg6) cells ( n = 4–7/group) ( F ); or 2 × 10 5 MC38 control or MC38- Cd155 –KO (sg2 and sg6) cells ( n = 7/group) ( G ). Metastatic burden in the lungs was quantified by counting colonies on the lung surface 14 days after tumor inoculation. ( H and I ) Female BALB/c WT mice were injected into the mammary fat pad with 5 × 10 4 4T1.2 control or 4T1.2- Cd155 –KO cells, and tumors were resected on day 14. In 1 group, the metastatic burden was quantified in the lungs by counting colonies on the lung surface on day 30 ( n = 9/group) ( H ), and in another group, the survival was monitored ( I ) ( n = 14–20/group; experiment was performed twice). * P

    Techniques Used: Mouse Assay, Injection

    Deletion of CD155 from host and tumor enhances the suppression of tumor progression. ( A ) Experimental protocol for the induction of primary s.c. or lung metastases with control or Cd155 -KO (sg2 and/or sg6) tumor cells in WT or Cd155 –/– mice. ( B ) WT and Cd155 –/– mice were injected i.v. with 1 × 10 5 B16F10 control, B16F10- Cd155 –KO (sg2), or B16F10- Cd155 –KO (sg6) cells ( n = 5–6/group). Metastatic burden was quantified in the lungs by counting colonies on the lung surface 14 days after tumor cell inoculation (the experiment was performed once). ( C ) WT and Cd155 –/– mice were injected i.v. with 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg6) cells ( n = 7–10/group). Fourteen days after tumor inoculation, the metastatic burden was quantified in the lungs by counting colonies on the lung surface (the experiment was performed once). ( D – F ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group) ( D ); 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg6) cells ( n = 8–9/group) ( E ); or 5 × 10 5 MC38 control or MC38- Cd155 –KO (sg6) cells ( n = 5/group) ( F ), and tumor sizes were measured at the indicated time points. ( G ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group). A dose of 250 μg cIg (clone 1-1) or anti–DNAM-1 (clone 480.1) mAb was injected on days –1, 0, and 7, relative to tumor inoculation (experiment was performed once). * P
    Figure Legend Snippet: Deletion of CD155 from host and tumor enhances the suppression of tumor progression. ( A ) Experimental protocol for the induction of primary s.c. or lung metastases with control or Cd155 -KO (sg2 and/or sg6) tumor cells in WT or Cd155 –/– mice. ( B ) WT and Cd155 –/– mice were injected i.v. with 1 × 10 5 B16F10 control, B16F10- Cd155 –KO (sg2), or B16F10- Cd155 –KO (sg6) cells ( n = 5–6/group). Metastatic burden was quantified in the lungs by counting colonies on the lung surface 14 days after tumor cell inoculation (the experiment was performed once). ( C ) WT and Cd155 –/– mice were injected i.v. with 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg6) cells ( n = 7–10/group). Fourteen days after tumor inoculation, the metastatic burden was quantified in the lungs by counting colonies on the lung surface (the experiment was performed once). ( D – F ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group) ( D ); 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg6) cells ( n = 8–9/group) ( E ); or 5 × 10 5 MC38 control or MC38- Cd155 –KO (sg6) cells ( n = 5/group) ( F ), and tumor sizes were measured at the indicated time points. ( G ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group). A dose of 250 μg cIg (clone 1-1) or anti–DNAM-1 (clone 480.1) mAb was injected on days –1, 0, and 7, relative to tumor inoculation (experiment was performed once). * P

    Techniques Used: Mouse Assay, Injection

    CD155 is expressed in malignant cells and tumor-infiltrating myeloid cells in human and mouse tumors. ( A and B ) Representative multiplexed IHC images of human primary cutaneous melanoma samples. CD155 (green) was distributed broadly within the carcinoma element of human melanoma, identified by HMB45 positivity (orange). Tumor-infiltrating myeloid cells were revealed by CD14 (red) or CD11c (yellow) positivity. The dotted line circumscribes HMB45 + tumor cells in a representative human melanoma TMA core. The merged image shows high colocalization of CD155 and HMB45. Scale bars: 200 μm ( A ) and 50 μm ( B ). ( C ) Colocalization of CD155 in tumor-infiltrating myeloid cells in human melanoma. CD11c (yellow) and CD14 (red) discriminated different populations of tumor-infiltrating cells, including CD11c + CD14 – DCs (yellow arrows), CD11c + CD14 + myeloid cells (white arrows), and CD11c – CD14 + monocytes/macrophages (red arrows). CD155 staining (green) was colocalized within each of these myeloid populations, as indicated in the merged panel. Scale bar: 50 μm. ( A – C ) Nuclei were stained with DAPI (blue) in each panel. ( D and E ) WT mice were injected s.c. with 1 × 10 5 B16F10 cells ( n = 5/group), and tumor samples were digested and analyzed on day 12. Tumor cells were gated by FSC hi SSC hi Zombie-yellow – CD45.2 – expression. ( D ) CD155 and PD-L1 expression on ex vivo B16F10 tumor cells is shown. ( E ) CD11b + CD11c + and CD11b + CD11c – tumor-infiltrating myeloid cell populations were gated by FSC lo SSC lo Zombie-yellow – CD45.2 + .
    Figure Legend Snippet: CD155 is expressed in malignant cells and tumor-infiltrating myeloid cells in human and mouse tumors. ( A and B ) Representative multiplexed IHC images of human primary cutaneous melanoma samples. CD155 (green) was distributed broadly within the carcinoma element of human melanoma, identified by HMB45 positivity (orange). Tumor-infiltrating myeloid cells were revealed by CD14 (red) or CD11c (yellow) positivity. The dotted line circumscribes HMB45 + tumor cells in a representative human melanoma TMA core. The merged image shows high colocalization of CD155 and HMB45. Scale bars: 200 μm ( A ) and 50 μm ( B ). ( C ) Colocalization of CD155 in tumor-infiltrating myeloid cells in human melanoma. CD11c (yellow) and CD14 (red) discriminated different populations of tumor-infiltrating cells, including CD11c + CD14 – DCs (yellow arrows), CD11c + CD14 + myeloid cells (white arrows), and CD11c – CD14 + monocytes/macrophages (red arrows). CD155 staining (green) was colocalized within each of these myeloid populations, as indicated in the merged panel. Scale bar: 50 μm. ( A – C ) Nuclei were stained with DAPI (blue) in each panel. ( D and E ) WT mice were injected s.c. with 1 × 10 5 B16F10 cells ( n = 5/group), and tumor samples were digested and analyzed on day 12. Tumor cells were gated by FSC hi SSC hi Zombie-yellow – CD45.2 – expression. ( D ) CD155 and PD-L1 expression on ex vivo B16F10 tumor cells is shown. ( E ) CD11b + CD11c + and CD11b + CD11c – tumor-infiltrating myeloid cell populations were gated by FSC lo SSC lo Zombie-yellow – CD45.2 + .

    Techniques Used: Immunohistochemistry, Staining, Mouse Assay, Injection, Expressing, Ex Vivo

    Related Articles

    Transfection:

    Article Title: CD155 loss enhances tumor suppression via combined host and tumor-intrinsic mechanisms
    Article Snippet: .. B16F10- Cd155 –KO (sg6) cells were transfected with a CD155 plasmid (pCMV3-mPVR, Sino Biological, catalog MG50259-UT), and CD155+ cells were sorted 2 days after transfection. .. The sorted CD155+ cells were then cultured in 200 μg/ml hygromycin B for 3 weeks to produce cells with stable expression of murine CD155.

    Plasmid Preparation:

    Article Title: CD155 loss enhances tumor suppression via combined host and tumor-intrinsic mechanisms
    Article Snippet: .. B16F10- Cd155 –KO (sg6) cells were transfected with a CD155 plasmid (pCMV3-mPVR, Sino Biological, catalog MG50259-UT), and CD155+ cells were sorted 2 days after transfection. .. The sorted CD155+ cells were then cultured in 200 μg/ml hygromycin B for 3 weeks to produce cells with stable expression of murine CD155.

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    Sino Biological cd155 plasmid
    Tumor-intrinsic <t>CD155</t> is critical for tumor cell migration and survival. ( A and B ) WT and Rag2 –/– γc –/– mice were injected s.c. with 2 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg2 and sg6) cells ( n = 6/group) ( A ), or 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg2 and sg6) cells ( n = 5–6/group) ( B ), and tumor sizes were measured at the indicated time points (the experiment was performed once). ( C and D ) Rag2 –/– γc –/– mice were injected i.v. with 5 × 10 4 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group) ( C ), or 1 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg6) cells ( n = 6/group) ( D ), and the metastatic burden was quantified in the lungs by counting colonies on the lung surface 14 days after tumor cell inoculation. ( E ) B16F10 control and B16F10- Cd155 –KO (sg6) cells (200 cells/well; n = 3/group) were cultured in 6-well plates for 6 days and stained with crystal violet to assess relative CFU. Images of the colonies of B16F10 control and B16F10- CD155 –KO (sg6) cells are shown, and the relative CFU was assessed (representative of 3 experiments). ( F and G ) B16F10 control or B16F10- CD155 –KO (sg6) cells (1 × 10 5 cells/well) were cultured in 96-well plates. Wounds were made, and wound-healing images were monitored and analyzed, and the percentage of relative wound closure was determined. ( H and I ) B16F10 control and B16F10- CD155 –KO (sg6) cells (1 × 10 5 cells/well) were cultured in 24-well plates under normoxic or hypoxic conditions ( n = 4/group) ( H ) or in media supplemented with 10% or 1% serum ( n = 4/group) ( I ), and apoptosis was evaluated 48 hours later with annexin V and 7-AAD. ( H and I ) Graphs show the representative rate of cell death. * P
    Cd155 Plasmid, supplied by Sino Biological, used in various techniques. Bioz Stars score: 91/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Sino Biological cd18 cdna orf clone mouse untagged
    Tumor-intrinsic <t>CD155</t> is critical for tumor cell migration and survival. ( A and B ) WT and Rag2 –/– γc –/– mice were injected s.c. with 2 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg2 and sg6) cells ( n = 6/group) ( A ), or 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg2 and sg6) cells ( n = 5–6/group) ( B ), and tumor sizes were measured at the indicated time points (the experiment was performed once). ( C and D ) Rag2 –/– γc –/– mice were injected i.v. with 5 × 10 4 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group) ( C ), or 1 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg6) cells ( n = 6/group) ( D ), and the metastatic burden was quantified in the lungs by counting colonies on the lung surface 14 days after tumor cell inoculation. ( E ) B16F10 control and B16F10- Cd155 –KO (sg6) cells (200 cells/well; n = 3/group) were cultured in 6-well plates for 6 days and stained with crystal violet to assess relative CFU. Images of the colonies of B16F10 control and B16F10- CD155 –KO (sg6) cells are shown, and the relative CFU was assessed (representative of 3 experiments). ( F and G ) B16F10 control or B16F10- CD155 –KO (sg6) cells (1 × 10 5 cells/well) were cultured in 96-well plates. Wounds were made, and wound-healing images were monitored and analyzed, and the percentage of relative wound closure was determined. ( H and I ) B16F10 control and B16F10- CD155 –KO (sg6) cells (1 × 10 5 cells/well) were cultured in 24-well plates under normoxic or hypoxic conditions ( n = 4/group) ( H ) or in media supplemented with 10% or 1% serum ( n = 4/group) ( I ), and apoptosis was evaluated 48 hours later with annexin V and 7-AAD. ( H and I ) Graphs show the representative rate of cell death. * P
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    Tumor-intrinsic CD155 is critical for tumor cell migration and survival. ( A and B ) WT and Rag2 –/– γc –/– mice were injected s.c. with 2 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg2 and sg6) cells ( n = 6/group) ( A ), or 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg2 and sg6) cells ( n = 5–6/group) ( B ), and tumor sizes were measured at the indicated time points (the experiment was performed once). ( C and D ) Rag2 –/– γc –/– mice were injected i.v. with 5 × 10 4 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group) ( C ), or 1 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg6) cells ( n = 6/group) ( D ), and the metastatic burden was quantified in the lungs by counting colonies on the lung surface 14 days after tumor cell inoculation. ( E ) B16F10 control and B16F10- Cd155 –KO (sg6) cells (200 cells/well; n = 3/group) were cultured in 6-well plates for 6 days and stained with crystal violet to assess relative CFU. Images of the colonies of B16F10 control and B16F10- CD155 –KO (sg6) cells are shown, and the relative CFU was assessed (representative of 3 experiments). ( F and G ) B16F10 control or B16F10- CD155 –KO (sg6) cells (1 × 10 5 cells/well) were cultured in 96-well plates. Wounds were made, and wound-healing images were monitored and analyzed, and the percentage of relative wound closure was determined. ( H and I ) B16F10 control and B16F10- CD155 –KO (sg6) cells (1 × 10 5 cells/well) were cultured in 24-well plates under normoxic or hypoxic conditions ( n = 4/group) ( H ) or in media supplemented with 10% or 1% serum ( n = 4/group) ( I ), and apoptosis was evaluated 48 hours later with annexin V and 7-AAD. ( H and I ) Graphs show the representative rate of cell death. * P

    Journal: The Journal of Clinical Investigation

    Article Title: CD155 loss enhances tumor suppression via combined host and tumor-intrinsic mechanisms

    doi: 10.1172/JCI98769

    Figure Lengend Snippet: Tumor-intrinsic CD155 is critical for tumor cell migration and survival. ( A and B ) WT and Rag2 –/– γc –/– mice were injected s.c. with 2 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg2 and sg6) cells ( n = 6/group) ( A ), or 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg2 and sg6) cells ( n = 5–6/group) ( B ), and tumor sizes were measured at the indicated time points (the experiment was performed once). ( C and D ) Rag2 –/– γc –/– mice were injected i.v. with 5 × 10 4 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group) ( C ), or 1 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg6) cells ( n = 6/group) ( D ), and the metastatic burden was quantified in the lungs by counting colonies on the lung surface 14 days after tumor cell inoculation. ( E ) B16F10 control and B16F10- Cd155 –KO (sg6) cells (200 cells/well; n = 3/group) were cultured in 6-well plates for 6 days and stained with crystal violet to assess relative CFU. Images of the colonies of B16F10 control and B16F10- CD155 –KO (sg6) cells are shown, and the relative CFU was assessed (representative of 3 experiments). ( F and G ) B16F10 control or B16F10- CD155 –KO (sg6) cells (1 × 10 5 cells/well) were cultured in 96-well plates. Wounds were made, and wound-healing images were monitored and analyzed, and the percentage of relative wound closure was determined. ( H and I ) B16F10 control and B16F10- CD155 –KO (sg6) cells (1 × 10 5 cells/well) were cultured in 24-well plates under normoxic or hypoxic conditions ( n = 4/group) ( H ) or in media supplemented with 10% or 1% serum ( n = 4/group) ( I ), and apoptosis was evaluated 48 hours later with annexin V and 7-AAD. ( H and I ) Graphs show the representative rate of cell death. * P

    Article Snippet: B16F10- Cd155 –KO (sg6) cells were transfected with a CD155 plasmid (pCMV3-mPVR, Sino Biological, catalog MG50259-UT), and CD155+ cells were sorted 2 days after transfection.

    Techniques: Migration, Mouse Assay, Injection, Cell Culture, Staining

    Blockade of PD-1 pathway combined with CD155 deletion enhances tumor growth suppression. ( A ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 6 MCA1956 cells ( n = 10/group). cIg or anti–PD-1 mAb (50 μg) was injected on days 8, 12, 16, and 20, relative to tumor inoculation. ( B ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 MC38 cells ( n = 5–6/group). cIg or anti-PD1 mAb (250 μg) was injected on days 8, 12, 16, and 20, relative to tumor inoculation. ( C ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group). Mice were injected with 250 μg cIg or anti–PD-1/CTLA4 mAb on days 12, 15, 18, and 21, relative to tumor inoculation. ( D ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group). cIg or anti–PD-1 and anti-CTLA4 mAbs (250 μg) were injected into WT mice with B16F10 control cells on days 8, 10, 12, and 14; WT mice with B16F10- Cd155 –KO (sg6) cells on days 12, 14, 16, and 18; Cd155 –/– mice with B16F10 control cells into on days 13, 15, 17, and 19; Cd155 –/– mice with B16F10- Cd155 –KO (sg6) cells on days 17, 19, 21, and 23, relative to tumor inoculation. ( E ) WT mice were injected s.c. with 1 × 10 5 B16F10 control (left) or B16F10- Cd155 –KO (sg6) (right) cells ( n = 5/group). A dose of 250 μg cIg, anti–PD-1 or anti-TIGIT and anti-CD96, or a combination of these mAbs was injected i.p. into WT mice with B16F10 control tumors on days 8, 10, 12, and 14 and into mice with B16F10- Cd155 –KO (sg6) tumors on days 10, 12, 14, and 16, relative to tumor inoculation. ( A – E ) Tumor sizes were measured at the indicated time points. ** P

    Journal: The Journal of Clinical Investigation

    Article Title: CD155 loss enhances tumor suppression via combined host and tumor-intrinsic mechanisms

    doi: 10.1172/JCI98769

    Figure Lengend Snippet: Blockade of PD-1 pathway combined with CD155 deletion enhances tumor growth suppression. ( A ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 6 MCA1956 cells ( n = 10/group). cIg or anti–PD-1 mAb (50 μg) was injected on days 8, 12, 16, and 20, relative to tumor inoculation. ( B ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 MC38 cells ( n = 5–6/group). cIg or anti-PD1 mAb (250 μg) was injected on days 8, 12, 16, and 20, relative to tumor inoculation. ( C ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group). Mice were injected with 250 μg cIg or anti–PD-1/CTLA4 mAb on days 12, 15, 18, and 21, relative to tumor inoculation. ( D ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group). cIg or anti–PD-1 and anti-CTLA4 mAbs (250 μg) were injected into WT mice with B16F10 control cells on days 8, 10, 12, and 14; WT mice with B16F10- Cd155 –KO (sg6) cells on days 12, 14, 16, and 18; Cd155 –/– mice with B16F10 control cells into on days 13, 15, 17, and 19; Cd155 –/– mice with B16F10- Cd155 –KO (sg6) cells on days 17, 19, 21, and 23, relative to tumor inoculation. ( E ) WT mice were injected s.c. with 1 × 10 5 B16F10 control (left) or B16F10- Cd155 –KO (sg6) (right) cells ( n = 5/group). A dose of 250 μg cIg, anti–PD-1 or anti-TIGIT and anti-CD96, or a combination of these mAbs was injected i.p. into WT mice with B16F10 control tumors on days 8, 10, 12, and 14 and into mice with B16F10- Cd155 –KO (sg6) tumors on days 10, 12, 14, and 16, relative to tumor inoculation. ( A – E ) Tumor sizes were measured at the indicated time points. ** P

    Article Snippet: B16F10- Cd155 –KO (sg6) cells were transfected with a CD155 plasmid (pCMV3-mPVR, Sino Biological, catalog MG50259-UT), and CD155+ cells were sorted 2 days after transfection.

    Techniques: Mouse Assay, Injection

    Tumor growth and metastasis are inhibited in Cd155 –/– mice in a BM cell–dependent manner. ( A – C ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 cells ( n = 6–7/group) ( A ) or 5 × 10 5 SM1WT1 cells ( n = 7/group) ( B ), or 5 × 10 5 MC38 cells ( n = 5–6/group) ( C ), and tumor sizes were measured at the indicated time points. ( D and E ) WT and Cd155 –/– mice were challenged i.v. with 2 × 10 5 B16F10 cells ( n = 8–11/group) ( D ) or 7.5 × 10 5 LWT1 cells ( n = 6–7/group) ( E ), 2 weeks after tumor inoculation, and metastatic burden was quantified in the lungs by counting colonies on the lung surface. ( F and G ) WT and Cd155 –/– mice were treated with 100 μg cIg, or 100 μg anti-CD8β (53.5.8, CD8 + T cell depletion), or 100 μg anti-CD4 (GK1.5, CD4 + T cell depletion) plus 100 μg anti-CD8β (53.5.8), or 50 μg anti-asGM1 (NK cell depletion) on days –1, 0, 7, and 14 for tumor growth, or on days –1, 0, and 7 for tumor metastasis relative to tumor inoculation. Mice were challenged s.c. with 1 × 10 5 B16F10 cells ( n = 5–6/group; the experiment was performed once) ( F ), and tumor sizes were measured at the indicated time points, or mice were challenged i.v. with 7.5 × 10 5 LWT1 cells ( n = 6/group) ( G ), and lung metastases were quantified 2 weeks after tumor inoculation. ( H and J ) Ptprc a (CD45.1 + ) and Cd155 –/– (CD45.2 + ) mice were irradiated twice (total radiation dose: 1,050 cGy/rad), and 5 × 10 6 BM cells from Ptprc a or Cd155 –/– mice were then i.v. injected into each irradiated mouse to construct BM chimeric mice ( H ). Mice were then challenged s.c. with 1 × 10 5 B16F10 ( I ) or i.v. with 2 × 10 5 B16F10 ( J ) cells, respectively ( n = 10/group; the experiment was performed once for both I and J ). Tumor sizes were measured at the indicated time points ( I ), and lung metastases were quantified 2 weeks after tumor inoculation ( J ). * P

    Journal: The Journal of Clinical Investigation

    Article Title: CD155 loss enhances tumor suppression via combined host and tumor-intrinsic mechanisms

    doi: 10.1172/JCI98769

    Figure Lengend Snippet: Tumor growth and metastasis are inhibited in Cd155 –/– mice in a BM cell–dependent manner. ( A – C ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 cells ( n = 6–7/group) ( A ) or 5 × 10 5 SM1WT1 cells ( n = 7/group) ( B ), or 5 × 10 5 MC38 cells ( n = 5–6/group) ( C ), and tumor sizes were measured at the indicated time points. ( D and E ) WT and Cd155 –/– mice were challenged i.v. with 2 × 10 5 B16F10 cells ( n = 8–11/group) ( D ) or 7.5 × 10 5 LWT1 cells ( n = 6–7/group) ( E ), 2 weeks after tumor inoculation, and metastatic burden was quantified in the lungs by counting colonies on the lung surface. ( F and G ) WT and Cd155 –/– mice were treated with 100 μg cIg, or 100 μg anti-CD8β (53.5.8, CD8 + T cell depletion), or 100 μg anti-CD4 (GK1.5, CD4 + T cell depletion) plus 100 μg anti-CD8β (53.5.8), or 50 μg anti-asGM1 (NK cell depletion) on days –1, 0, 7, and 14 for tumor growth, or on days –1, 0, and 7 for tumor metastasis relative to tumor inoculation. Mice were challenged s.c. with 1 × 10 5 B16F10 cells ( n = 5–6/group; the experiment was performed once) ( F ), and tumor sizes were measured at the indicated time points, or mice were challenged i.v. with 7.5 × 10 5 LWT1 cells ( n = 6/group) ( G ), and lung metastases were quantified 2 weeks after tumor inoculation. ( H and J ) Ptprc a (CD45.1 + ) and Cd155 –/– (CD45.2 + ) mice were irradiated twice (total radiation dose: 1,050 cGy/rad), and 5 × 10 6 BM cells from Ptprc a or Cd155 –/– mice were then i.v. injected into each irradiated mouse to construct BM chimeric mice ( H ). Mice were then challenged s.c. with 1 × 10 5 B16F10 ( I ) or i.v. with 2 × 10 5 B16F10 ( J ) cells, respectively ( n = 10/group; the experiment was performed once for both I and J ). Tumor sizes were measured at the indicated time points ( I ), and lung metastases were quantified 2 weeks after tumor inoculation ( J ). * P

    Article Snippet: B16F10- Cd155 –KO (sg6) cells were transfected with a CD155 plasmid (pCMV3-mPVR, Sino Biological, catalog MG50259-UT), and CD155+ cells were sorted 2 days after transfection.

    Techniques: Mouse Assay, Injection, Irradiation, Construct

    Inhibition of tumor growth and metastasis in Cd155 –/– mice is DNAM-1 dependent. ( A ) DNAM-1, CD96, and TIGIT expression was analyzed on day 12 on tumor-infiltrating CD4 + T cells, CD8 + T cells, and NK cells after inoculation of 1 × 10 5 B16F10 cells in WT and CD155 –/– mice ( n = 5/group). The mean fluorescence intensity (MFI) is shown. ( B ) Tumor sizes were measured at the indicated time points for WT and Cd155 –/– mice ( n = 5–6/group) treated with 100 μg cIg, 100 μg anti-CD8β (clone 53.5.8), 250 μg anti-DNAM-1 (clone 480.1), or 50 μg anti-asGM1 on days –1, 0, 7, and 14, relative to inoculation of 1 × 10 5 B16F10 cells (the experiment was performed twice). ( C ) Splenocytes from naive C57BL/6 WT and Cd155 –/– mice ( n = 3) were stimulated with 1 μg/ml anti-CD3 and 2 μg/ml anti-CD28 for 24 hours, and the expression of IFN-γ on CD8 + T cells was analyzed by flow cytometry (data are representative of 2 experiments). ( D ) WT and Cd155 –/– mice ( n = 5/group) were injected i.v. with 1 × 10 5 B16F10 melanoma cells and treated on days –1, 0, and 7, relative to tumor inoculation with 250 μg cIg (clone 1-1), 250 μg anti–DNAM-1 (clone 480.1), or 50 μg anti-asGM1. Metastatic burden was quantified in the lungs by counting colonies on the lung surface 14 days after tumor cell inoculation ( n = 5/group; the experiment was performed once). ( E ) NK cells from the spleens of naive C57BL/6 WT and Cd155 –/– mice ( n = 4) were purified and stimulated with the indicated concentrations of IL-12 and IL-18 for 24 hours, and the expression of IFN-γ on NK cells was analyzed by flow cytometry. * P

    Journal: The Journal of Clinical Investigation

    Article Title: CD155 loss enhances tumor suppression via combined host and tumor-intrinsic mechanisms

    doi: 10.1172/JCI98769

    Figure Lengend Snippet: Inhibition of tumor growth and metastasis in Cd155 –/– mice is DNAM-1 dependent. ( A ) DNAM-1, CD96, and TIGIT expression was analyzed on day 12 on tumor-infiltrating CD4 + T cells, CD8 + T cells, and NK cells after inoculation of 1 × 10 5 B16F10 cells in WT and CD155 –/– mice ( n = 5/group). The mean fluorescence intensity (MFI) is shown. ( B ) Tumor sizes were measured at the indicated time points for WT and Cd155 –/– mice ( n = 5–6/group) treated with 100 μg cIg, 100 μg anti-CD8β (clone 53.5.8), 250 μg anti-DNAM-1 (clone 480.1), or 50 μg anti-asGM1 on days –1, 0, 7, and 14, relative to inoculation of 1 × 10 5 B16F10 cells (the experiment was performed twice). ( C ) Splenocytes from naive C57BL/6 WT and Cd155 –/– mice ( n = 3) were stimulated with 1 μg/ml anti-CD3 and 2 μg/ml anti-CD28 for 24 hours, and the expression of IFN-γ on CD8 + T cells was analyzed by flow cytometry (data are representative of 2 experiments). ( D ) WT and Cd155 –/– mice ( n = 5/group) were injected i.v. with 1 × 10 5 B16F10 melanoma cells and treated on days –1, 0, and 7, relative to tumor inoculation with 250 μg cIg (clone 1-1), 250 μg anti–DNAM-1 (clone 480.1), or 50 μg anti-asGM1. Metastatic burden was quantified in the lungs by counting colonies on the lung surface 14 days after tumor cell inoculation ( n = 5/group; the experiment was performed once). ( E ) NK cells from the spleens of naive C57BL/6 WT and Cd155 –/– mice ( n = 4) were purified and stimulated with the indicated concentrations of IL-12 and IL-18 for 24 hours, and the expression of IFN-γ on NK cells was analyzed by flow cytometry. * P

    Article Snippet: B16F10- Cd155 –KO (sg6) cells were transfected with a CD155 plasmid (pCMV3-mPVR, Sino Biological, catalog MG50259-UT), and CD155+ cells were sorted 2 days after transfection.

    Techniques: Inhibition, Mouse Assay, Expressing, Fluorescence, Flow Cytometry, Cytometry, Injection, Purification

    Deletion of tumor CD155 decreases tumor growth and metastasis. ( A – D ) WT mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg2 and sg6) cells ( n = 6/group) ( A ); 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg2 and sg6) cells ( n = 5–6/group) ( B ); 5 × 10 5 MC38 control or MC38- Cd155 –KO (sg2 and sg6) cells ( n = 5/group) ( C ); or 1 × 10 6 MCA1956 control or MCA1956- Cd155 –KO (sg6) cells ( n = 5/group) ( D ), and tumor sizes were measured at the indicated time points. ( E – G ) WT mice were injected i.v. with 2 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5–6/group) ( E ); 7.5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg2 and sg6) cells ( n = 4–7/group) ( F ); or 2 × 10 5 MC38 control or MC38- Cd155 –KO (sg2 and sg6) cells ( n = 7/group) ( G ). Metastatic burden in the lungs was quantified by counting colonies on the lung surface 14 days after tumor inoculation. ( H and I ) Female BALB/c WT mice were injected into the mammary fat pad with 5 × 10 4 4T1.2 control or 4T1.2- Cd155 –KO cells, and tumors were resected on day 14. In 1 group, the metastatic burden was quantified in the lungs by counting colonies on the lung surface on day 30 ( n = 9/group) ( H ), and in another group, the survival was monitored ( I ) ( n = 14–20/group; experiment was performed twice). * P

    Journal: The Journal of Clinical Investigation

    Article Title: CD155 loss enhances tumor suppression via combined host and tumor-intrinsic mechanisms

    doi: 10.1172/JCI98769

    Figure Lengend Snippet: Deletion of tumor CD155 decreases tumor growth and metastasis. ( A – D ) WT mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg2 and sg6) cells ( n = 6/group) ( A ); 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg2 and sg6) cells ( n = 5–6/group) ( B ); 5 × 10 5 MC38 control or MC38- Cd155 –KO (sg2 and sg6) cells ( n = 5/group) ( C ); or 1 × 10 6 MCA1956 control or MCA1956- Cd155 –KO (sg6) cells ( n = 5/group) ( D ), and tumor sizes were measured at the indicated time points. ( E – G ) WT mice were injected i.v. with 2 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5–6/group) ( E ); 7.5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg2 and sg6) cells ( n = 4–7/group) ( F ); or 2 × 10 5 MC38 control or MC38- Cd155 –KO (sg2 and sg6) cells ( n = 7/group) ( G ). Metastatic burden in the lungs was quantified by counting colonies on the lung surface 14 days after tumor inoculation. ( H and I ) Female BALB/c WT mice were injected into the mammary fat pad with 5 × 10 4 4T1.2 control or 4T1.2- Cd155 –KO cells, and tumors were resected on day 14. In 1 group, the metastatic burden was quantified in the lungs by counting colonies on the lung surface on day 30 ( n = 9/group) ( H ), and in another group, the survival was monitored ( I ) ( n = 14–20/group; experiment was performed twice). * P

    Article Snippet: B16F10- Cd155 –KO (sg6) cells were transfected with a CD155 plasmid (pCMV3-mPVR, Sino Biological, catalog MG50259-UT), and CD155+ cells were sorted 2 days after transfection.

    Techniques: Mouse Assay, Injection

    Deletion of CD155 from host and tumor enhances the suppression of tumor progression. ( A ) Experimental protocol for the induction of primary s.c. or lung metastases with control or Cd155 -KO (sg2 and/or sg6) tumor cells in WT or Cd155 –/– mice. ( B ) WT and Cd155 –/– mice were injected i.v. with 1 × 10 5 B16F10 control, B16F10- Cd155 –KO (sg2), or B16F10- Cd155 –KO (sg6) cells ( n = 5–6/group). Metastatic burden was quantified in the lungs by counting colonies on the lung surface 14 days after tumor cell inoculation (the experiment was performed once). ( C ) WT and Cd155 –/– mice were injected i.v. with 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg6) cells ( n = 7–10/group). Fourteen days after tumor inoculation, the metastatic burden was quantified in the lungs by counting colonies on the lung surface (the experiment was performed once). ( D – F ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group) ( D ); 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg6) cells ( n = 8–9/group) ( E ); or 5 × 10 5 MC38 control or MC38- Cd155 –KO (sg6) cells ( n = 5/group) ( F ), and tumor sizes were measured at the indicated time points. ( G ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group). A dose of 250 μg cIg (clone 1-1) or anti–DNAM-1 (clone 480.1) mAb was injected on days –1, 0, and 7, relative to tumor inoculation (experiment was performed once). * P

    Journal: The Journal of Clinical Investigation

    Article Title: CD155 loss enhances tumor suppression via combined host and tumor-intrinsic mechanisms

    doi: 10.1172/JCI98769

    Figure Lengend Snippet: Deletion of CD155 from host and tumor enhances the suppression of tumor progression. ( A ) Experimental protocol for the induction of primary s.c. or lung metastases with control or Cd155 -KO (sg2 and/or sg6) tumor cells in WT or Cd155 –/– mice. ( B ) WT and Cd155 –/– mice were injected i.v. with 1 × 10 5 B16F10 control, B16F10- Cd155 –KO (sg2), or B16F10- Cd155 –KO (sg6) cells ( n = 5–6/group). Metastatic burden was quantified in the lungs by counting colonies on the lung surface 14 days after tumor cell inoculation (the experiment was performed once). ( C ) WT and Cd155 –/– mice were injected i.v. with 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg6) cells ( n = 7–10/group). Fourteen days after tumor inoculation, the metastatic burden was quantified in the lungs by counting colonies on the lung surface (the experiment was performed once). ( D – F ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group) ( D ); 5 × 10 5 LWT1 control or LWT1- Cd155 –KO (sg6) cells ( n = 8–9/group) ( E ); or 5 × 10 5 MC38 control or MC38- Cd155 –KO (sg6) cells ( n = 5/group) ( F ), and tumor sizes were measured at the indicated time points. ( G ) WT and Cd155 –/– mice were injected s.c. with 1 × 10 5 B16F10 control or B16F10- Cd155 –KO (sg6) cells ( n = 5/group). A dose of 250 μg cIg (clone 1-1) or anti–DNAM-1 (clone 480.1) mAb was injected on days –1, 0, and 7, relative to tumor inoculation (experiment was performed once). * P

    Article Snippet: B16F10- Cd155 –KO (sg6) cells were transfected with a CD155 plasmid (pCMV3-mPVR, Sino Biological, catalog MG50259-UT), and CD155+ cells were sorted 2 days after transfection.

    Techniques: Mouse Assay, Injection

    CD155 is expressed in malignant cells and tumor-infiltrating myeloid cells in human and mouse tumors. ( A and B ) Representative multiplexed IHC images of human primary cutaneous melanoma samples. CD155 (green) was distributed broadly within the carcinoma element of human melanoma, identified by HMB45 positivity (orange). Tumor-infiltrating myeloid cells were revealed by CD14 (red) or CD11c (yellow) positivity. The dotted line circumscribes HMB45 + tumor cells in a representative human melanoma TMA core. The merged image shows high colocalization of CD155 and HMB45. Scale bars: 200 μm ( A ) and 50 μm ( B ). ( C ) Colocalization of CD155 in tumor-infiltrating myeloid cells in human melanoma. CD11c (yellow) and CD14 (red) discriminated different populations of tumor-infiltrating cells, including CD11c + CD14 – DCs (yellow arrows), CD11c + CD14 + myeloid cells (white arrows), and CD11c – CD14 + monocytes/macrophages (red arrows). CD155 staining (green) was colocalized within each of these myeloid populations, as indicated in the merged panel. Scale bar: 50 μm. ( A – C ) Nuclei were stained with DAPI (blue) in each panel. ( D and E ) WT mice were injected s.c. with 1 × 10 5 B16F10 cells ( n = 5/group), and tumor samples were digested and analyzed on day 12. Tumor cells were gated by FSC hi SSC hi Zombie-yellow – CD45.2 – expression. ( D ) CD155 and PD-L1 expression on ex vivo B16F10 tumor cells is shown. ( E ) CD11b + CD11c + and CD11b + CD11c – tumor-infiltrating myeloid cell populations were gated by FSC lo SSC lo Zombie-yellow – CD45.2 + .

    Journal: The Journal of Clinical Investigation

    Article Title: CD155 loss enhances tumor suppression via combined host and tumor-intrinsic mechanisms

    doi: 10.1172/JCI98769

    Figure Lengend Snippet: CD155 is expressed in malignant cells and tumor-infiltrating myeloid cells in human and mouse tumors. ( A and B ) Representative multiplexed IHC images of human primary cutaneous melanoma samples. CD155 (green) was distributed broadly within the carcinoma element of human melanoma, identified by HMB45 positivity (orange). Tumor-infiltrating myeloid cells were revealed by CD14 (red) or CD11c (yellow) positivity. The dotted line circumscribes HMB45 + tumor cells in a representative human melanoma TMA core. The merged image shows high colocalization of CD155 and HMB45. Scale bars: 200 μm ( A ) and 50 μm ( B ). ( C ) Colocalization of CD155 in tumor-infiltrating myeloid cells in human melanoma. CD11c (yellow) and CD14 (red) discriminated different populations of tumor-infiltrating cells, including CD11c + CD14 – DCs (yellow arrows), CD11c + CD14 + myeloid cells (white arrows), and CD11c – CD14 + monocytes/macrophages (red arrows). CD155 staining (green) was colocalized within each of these myeloid populations, as indicated in the merged panel. Scale bar: 50 μm. ( A – C ) Nuclei were stained with DAPI (blue) in each panel. ( D and E ) WT mice were injected s.c. with 1 × 10 5 B16F10 cells ( n = 5/group), and tumor samples were digested and analyzed on day 12. Tumor cells were gated by FSC hi SSC hi Zombie-yellow – CD45.2 – expression. ( D ) CD155 and PD-L1 expression on ex vivo B16F10 tumor cells is shown. ( E ) CD11b + CD11c + and CD11b + CD11c – tumor-infiltrating myeloid cell populations were gated by FSC lo SSC lo Zombie-yellow – CD45.2 + .

    Article Snippet: B16F10- Cd155 –KO (sg6) cells were transfected with a CD155 plasmid (pCMV3-mPVR, Sino Biological, catalog MG50259-UT), and CD155+ cells were sorted 2 days after transfection.

    Techniques: Immunohistochemistry, Staining, Mouse Assay, Injection, Expressing, Ex Vivo