cd155 plasmid  (Sino Biological)


Bioz Verified Symbol Sino Biological is a verified supplier
Bioz Manufacturer Symbol Sino Biological manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 91
    Name:
    CD155 PVR cDNA ORF Clone Mouse untagged
    Description:
    Full length Clone DNA of Mouse poliovirus receptor
    Catalog Number:
    MG50259-UT
    Price:
    195.0
    Category:
    cDNA Clone
    Applications:
    Stable or Transient mammalian expression
    Size:
    1Unit
    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
    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 1 article reviews
    Price from $9.99 to $1999.99
    cd155 plasmid - by Bioz Stars, 2021-04
    91/100 stars

    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

    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.

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 91
    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 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cd155 plasmid/product/Sino Biological
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    cd155 plasmid - by Bioz Stars, 2021-04
    91/100 stars
      Buy from Supplier

    93
    Sino Biological human cd155 coding sequence
    The TIGIT and PD-1 ligands are expressed in NHL. Ligand expression was characterized by IHC and flow cytometry. A and B , IHC staining of DLBCL, MCL, and CLL frozen tissue sections using antibodies against <t>CD155,</t> CD112, PD-L1, and CD68. The tissue sections are closely neighbored to each other, enabling the comparison of identical structures. A , CD155 and CD112 are expressed by endothelial cells, whereas PD-L1 is found on macrophages, as confirmed by staining with the macrophage marker CD68. Image objective, ×20. B , MCL and DLBCL cases demonstrating CD155 expression in lymphoma cells (arrows on left and right), in addition to endothelial cells (arrow head, left) and intrasinusal histiocytes/macrophages (arrow heads, right). C , Flow cytometry analysis of CD155, CD112, and PD-L1/PD-L2 surface expression in tumor cells from FL ( n = 10), DLBCL ( n = 18), MCL ( n = 10), CLL ( n = 6), and MZL ( n = 2) and nonmalignant B cells from tonsils ( n = 8) analyzed by flow cytometry.
    Human Cd155 Coding Sequence, supplied by Sino Biological, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human cd155 coding sequence/product/Sino Biological
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    human cd155 coding sequence - by Bioz Stars, 2021-04
    93/100 stars
      Buy from Supplier

    92
    Sino Biological plasmid pcmv3 c ha cd155
    The TIGIT and PD-1 ligands are expressed in NHL. Ligand expression was characterized by IHC and flow cytometry. A and B , IHC staining of DLBCL, MCL, and CLL frozen tissue sections using antibodies against <t>CD155,</t> CD112, PD-L1, and CD68. The tissue sections are closely neighbored to each other, enabling the comparison of identical structures. A , CD155 and CD112 are expressed by endothelial cells, whereas PD-L1 is found on macrophages, as confirmed by staining with the macrophage marker CD68. Image objective, ×20. B , MCL and DLBCL cases demonstrating CD155 expression in lymphoma cells (arrows on left and right), in addition to endothelial cells (arrow head, left) and intrasinusal histiocytes/macrophages (arrow heads, right). C , Flow cytometry analysis of CD155, CD112, and PD-L1/PD-L2 surface expression in tumor cells from FL ( n = 10), DLBCL ( n = 18), MCL ( n = 10), CLL ( n = 6), and MZL ( n = 2) and nonmalignant B cells from tonsils ( n = 8) analyzed by flow cytometry.
    Plasmid Pcmv3 C Ha Cd155, supplied by Sino Biological, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/plasmid pcmv3 c ha cd155/product/Sino Biological
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    plasmid pcmv3 c ha cd155 - by Bioz Stars, 2021-04
    92/100 stars
      Buy from Supplier

    Image Search Results


    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

    The TIGIT and PD-1 ligands are expressed in NHL. Ligand expression was characterized by IHC and flow cytometry. A and B , IHC staining of DLBCL, MCL, and CLL frozen tissue sections using antibodies against CD155, CD112, PD-L1, and CD68. The tissue sections are closely neighbored to each other, enabling the comparison of identical structures. A , CD155 and CD112 are expressed by endothelial cells, whereas PD-L1 is found on macrophages, as confirmed by staining with the macrophage marker CD68. Image objective, ×20. B , MCL and DLBCL cases demonstrating CD155 expression in lymphoma cells (arrows on left and right), in addition to endothelial cells (arrow head, left) and intrasinusal histiocytes/macrophages (arrow heads, right). C , Flow cytometry analysis of CD155, CD112, and PD-L1/PD-L2 surface expression in tumor cells from FL ( n = 10), DLBCL ( n = 18), MCL ( n = 10), CLL ( n = 6), and MZL ( n = 2) and nonmalignant B cells from tonsils ( n = 8) analyzed by flow cytometry.

    Journal: Cancer immunology research

    Article Title: TIGIT and PD-1 Mark Intratumoral T Cells with Reduced Effector Function in B-cell Non-Hodgkin Lymphoma

    doi: 10.1158/2326-6066.CIR-18-0351

    Figure Lengend Snippet: The TIGIT and PD-1 ligands are expressed in NHL. Ligand expression was characterized by IHC and flow cytometry. A and B , IHC staining of DLBCL, MCL, and CLL frozen tissue sections using antibodies against CD155, CD112, PD-L1, and CD68. The tissue sections are closely neighbored to each other, enabling the comparison of identical structures. A , CD155 and CD112 are expressed by endothelial cells, whereas PD-L1 is found on macrophages, as confirmed by staining with the macrophage marker CD68. Image objective, ×20. B , MCL and DLBCL cases demonstrating CD155 expression in lymphoma cells (arrows on left and right), in addition to endothelial cells (arrow head, left) and intrasinusal histiocytes/macrophages (arrow heads, right). C , Flow cytometry analysis of CD155, CD112, and PD-L1/PD-L2 surface expression in tumor cells from FL ( n = 10), DLBCL ( n = 18), MCL ( n = 10), CLL ( n = 6), and MZL ( n = 2) and nonmalignant B cells from tonsils ( n = 8) analyzed by flow cytometry.

    Article Snippet: The human CD155 coding sequence was extracted from the commercial plasmid pCMV3-C-HA-CD155 (#HG10109-CY, Sino Biological) by PCR to remove the HA tag and to create the original isoform-1 using the following primers: 5′-CAC CAT GGC CCG AGC CAT G-3′ and 5′-GAA TTC ACC TTG TGC CCT CTG TCT GT-3′.

    Techniques: Expressing, Immunohistochemistry, Flow Cytometry, Cytometry, Staining, Marker

    A, Representative immunohistochemical images showing in situ CD155 expression in hepatocellular carcinoma sections from 10 patients. B, Representative immunofluorescence images showing CD155 expression in SNU423, Hep3B, and Bel-7402 cells. C, Flow cytometry plots showing CD155 expression in SNU423, Hep3B, and Bel-7402 cells. D, The 2-dimensional visualization of CD8 T-cell clusters of 5 patients by t-SNE. Each dot corresponds to a single cell. The depth of each dot color indicates the level of T-cell immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domain (TIGIT) expression. E, The violin plots showing the level of TIGIT expression in 5 CD8 T-cell clusters of all and individual patients. F, Representative immunofluorescence images showing the TIGIT + CD8 + T cells (white arrows) in hepatocellular carcinoma sections.

    Journal: Journal of Immunotherapy (Hagerstown, Md. : 1997)

    Article Title: TIGIT Can Exert Immunosuppressive Effects on CD8+ T Cells by the CD155/TIGIT Signaling Pathway for Hepatocellular Carcinoma In Vitro

    doi: 10.1097/CJI.0000000000000330

    Figure Lengend Snippet: A, Representative immunohistochemical images showing in situ CD155 expression in hepatocellular carcinoma sections from 10 patients. B, Representative immunofluorescence images showing CD155 expression in SNU423, Hep3B, and Bel-7402 cells. C, Flow cytometry plots showing CD155 expression in SNU423, Hep3B, and Bel-7402 cells. D, The 2-dimensional visualization of CD8 T-cell clusters of 5 patients by t-SNE. Each dot corresponds to a single cell. The depth of each dot color indicates the level of T-cell immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domain (TIGIT) expression. E, The violin plots showing the level of TIGIT expression in 5 CD8 T-cell clusters of all and individual patients. F, Representative immunofluorescence images showing the TIGIT + CD8 + T cells (white arrows) in hepatocellular carcinoma sections.

    Article Snippet: The functional anti-human TIGIT antibody (clone MBSA43, mouse IgG1; eBioscience, San Diego, CA) and recombinant human CD155/Fc protein (Sino Biological Inc., Beijing, China) were added to the culture medium, as appropriate.

    Techniques: Immunohistochemistry, In Situ, Expressing, Immunofluorescence, Flow Cytometry

    A, Amount of TNF-α, IL-17A, IFN-γ, and IL-10 secreted by CD8 + T cells cultured with 1 µg/mL CD155 with/out anti-TIGIT antibody. B, Amount of IL-17A, IFN-γ, IL-10, perforin, granzyme B, and granlysin produced by stimulated CD8 + T cells cocultured with Bel-7402 with/out anti-TIGIT antibody. C, Flow cytometry plots showing CD155 expression in Bel-7402-vector or Bel-7402-CD155 RNAi cells. D, Amount of TNF-α, IL-17A, IFN-γ, IL-10, perforin, and granlysin produced by stimulated CD8 + T cells cocultured with Bel-7402-vector or Bel-7402-CD155 RNAi cells with/out anti-TIGIT antibody. * P

    Journal: Journal of Immunotherapy (Hagerstown, Md. : 1997)

    Article Title: TIGIT Can Exert Immunosuppressive Effects on CD8+ T Cells by the CD155/TIGIT Signaling Pathway for Hepatocellular Carcinoma In Vitro

    doi: 10.1097/CJI.0000000000000330

    Figure Lengend Snippet: A, Amount of TNF-α, IL-17A, IFN-γ, and IL-10 secreted by CD8 + T cells cultured with 1 µg/mL CD155 with/out anti-TIGIT antibody. B, Amount of IL-17A, IFN-γ, IL-10, perforin, granzyme B, and granlysin produced by stimulated CD8 + T cells cocultured with Bel-7402 with/out anti-TIGIT antibody. C, Flow cytometry plots showing CD155 expression in Bel-7402-vector or Bel-7402-CD155 RNAi cells. D, Amount of TNF-α, IL-17A, IFN-γ, IL-10, perforin, and granlysin produced by stimulated CD8 + T cells cocultured with Bel-7402-vector or Bel-7402-CD155 RNAi cells with/out anti-TIGIT antibody. * P

    Article Snippet: The functional anti-human TIGIT antibody (clone MBSA43, mouse IgG1; eBioscience, San Diego, CA) and recombinant human CD155/Fc protein (Sino Biological Inc., Beijing, China) were added to the culture medium, as appropriate.

    Techniques: Cell Culture, Produced, Flow Cytometry, Expressing, Plasmid Preparation

    A, Mechanism of T-cell immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domain (TIGIT)/CD155-mediated suppression effects in natural killer cells. Upon interaction with CD155, the immunoglobulin tail tyrosine (ITT)-like motif of TIGIT is phosphorylated on Tyr225 and binds the cytosolic adaptor growth factor receptor-bound protein 2 (GRB2), which can recruit SH2 domain–containing inositol-5-phosphatase 1 (SHIP1) to inhibit phosphoinositide 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) signaling. In addition, phosphorylated TIGIT recruits SHIP1 through β-arrestin 2 and impairs nuclear factor-κB (NF-κB) activation by blocking tumor necrosis factor receptor–associated factor 6 (TRAF6) autoubiquitylation. B–D, Representative immunoblot showing AKT, p-AKT, ERK, p-ERK, and p-IκBα expression in stimulated T cells cocultured with SNU423, Bel-7402, and Bel-7402-CD155 RNAi cells with/out anti-TIGIT antibody. ERK indicates extracellular-regulated kinase; IFN, interferon; NK, natural killer.

    Journal: Journal of Immunotherapy (Hagerstown, Md. : 1997)

    Article Title: TIGIT Can Exert Immunosuppressive Effects on CD8+ T Cells by the CD155/TIGIT Signaling Pathway for Hepatocellular Carcinoma In Vitro

    doi: 10.1097/CJI.0000000000000330

    Figure Lengend Snippet: A, Mechanism of T-cell immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domain (TIGIT)/CD155-mediated suppression effects in natural killer cells. Upon interaction with CD155, the immunoglobulin tail tyrosine (ITT)-like motif of TIGIT is phosphorylated on Tyr225 and binds the cytosolic adaptor growth factor receptor-bound protein 2 (GRB2), which can recruit SH2 domain–containing inositol-5-phosphatase 1 (SHIP1) to inhibit phosphoinositide 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) signaling. In addition, phosphorylated TIGIT recruits SHIP1 through β-arrestin 2 and impairs nuclear factor-κB (NF-κB) activation by blocking tumor necrosis factor receptor–associated factor 6 (TRAF6) autoubiquitylation. B–D, Representative immunoblot showing AKT, p-AKT, ERK, p-ERK, and p-IκBα expression in stimulated T cells cocultured with SNU423, Bel-7402, and Bel-7402-CD155 RNAi cells with/out anti-TIGIT antibody. ERK indicates extracellular-regulated kinase; IFN, interferon; NK, natural killer.

    Article Snippet: The functional anti-human TIGIT antibody (clone MBSA43, mouse IgG1; eBioscience, San Diego, CA) and recombinant human CD155/Fc protein (Sino Biological Inc., Beijing, China) were added to the culture medium, as appropriate.

    Techniques: Activation Assay, Blocking Assay, Expressing