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anti mouse cd8a  (Bio X Cell)


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    Structured Review

    Bio X Cell anti mouse cd8a
    Proangiogenic and immunosuppression phenotype of TANs in the CRLM microenvironment. A, Heatmap showing signature scores for angiogenesis, myeloid cell recruitment, neutrophil cytotoxicity, MDSC, and NET across each TAN and PMN subset. B, Comparison of angiogenesis, myeloid cell recruitment, MDSC, and NET signature scores among TAN and PMN subsets. C, Dot plot illustrating expression levels of major cytokines and chemokines in each TAN and PMN subset. D, Representative IHC images of CD31 staining in CRLM tissues. Scale bars, 50 µm. E, Correlation analysis between CD31 and TAN1 density using Spearman’s rank correlation ( n = 102). F, Representative images and quantification of tube formation in HUVECs when cocultured with conditioned medium from human LGALS3 − neutrophils or LGALS3 + neutrophils ( n = 6). G, UMAP plot showing six monocyte/macrophage subsets across colorectal cancer, adjacent liver tissues, CRLM, and PB samples. H, Shell-like plot depicting ligand–receptor interaction strength between TAN1_LGASL3 and neutrophil/monocyte/macrophage subset in CRLM. I, Selected ligand–receptor interactions between TAN1_LGASL3 and neutrophil/monocyte/macrophage subset in CRLM. J, Representative mIHC images of CD68, CCL3L1, CD66b, CCR1, and BHLHE40 in CRLM. Scale bars, 50 µm. K, Representative images of macrophage migration assays and effects of conditioned medium from human LGALS3 + neutrophils on migration of macrophages (induced from THP-1 cells) in the presence of CCR1 inhibitor (BX471) or anti-CCL3 antibody ( n = 6). L, Comparison of immunosuppressive macrophage signature scores between colorectal cancer and CRLM. M, Schematic of the CRLM mouse model. C57BL/6 mice received intrasplenic injections of mouse colorectal cancer cells (MC38). Mice were subsequently treated with IgG control (IgG; n = 6), anti-Ly6G antibody (anti-Ly6G; n = 6), or anti-Ly6G plus <t>anti-CD8a</t> antibodies (anti-Ly6G + anti-CD8a; n = 6). Livers were harvested on day 14. N, Representative images of liver metastases from IgG, anti-Ly6G, and anti-Ly6G + anti-CD8a groups. O, Comparison of liver weights among the three groups. P values were calculated by the Wilcoxon rank-sum test ( B and L ) and unpaired Student t test ( F , K , and O ). *, P < 0.05; **, P < 0.01; ***, P < 0.001. CRC, colorectal cancer; Ctrl, control.
    Anti Mouse Cd8a, supplied by Bio X Cell, used in various techniques. Bioz Stars score: 97/100, based on 641 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/invivomab+anti+mouse+cd8a/InVivoMAb+anti-mouse+CD8%CE%B1/pmc13628106-246-7-9
    Average 97 stars, based on 641 article reviews
    anti mouse cd8a - by Bioz Stars, 2026-10
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    Images

    1) Product Images from "Senescent-Like Neutrophils Shape Angiogenic Immunosuppressive Niches in Colorectal Cancer Liver Metastasis"

    Article Title: Senescent-Like Neutrophils Shape Angiogenic Immunosuppressive Niches in Colorectal Cancer Liver Metastasis

    Journal: Cancer Discovery

    doi: 10.1158/2159-8290.CD-25-0820

    Proangiogenic and immunosuppression phenotype of TANs in the CRLM microenvironment. A, Heatmap showing signature scores for angiogenesis, myeloid cell recruitment, neutrophil cytotoxicity, MDSC, and NET across each TAN and PMN subset. B, Comparison of angiogenesis, myeloid cell recruitment, MDSC, and NET signature scores among TAN and PMN subsets. C, Dot plot illustrating expression levels of major cytokines and chemokines in each TAN and PMN subset. D, Representative IHC images of CD31 staining in CRLM tissues. Scale bars, 50 µm. E, Correlation analysis between CD31 and TAN1 density using Spearman’s rank correlation ( n = 102). F, Representative images and quantification of tube formation in HUVECs when cocultured with conditioned medium from human LGALS3 − neutrophils or LGALS3 + neutrophils ( n = 6). G, UMAP plot showing six monocyte/macrophage subsets across colorectal cancer, adjacent liver tissues, CRLM, and PB samples. H, Shell-like plot depicting ligand–receptor interaction strength between TAN1_LGASL3 and neutrophil/monocyte/macrophage subset in CRLM. I, Selected ligand–receptor interactions between TAN1_LGASL3 and neutrophil/monocyte/macrophage subset in CRLM. J, Representative mIHC images of CD68, CCL3L1, CD66b, CCR1, and BHLHE40 in CRLM. Scale bars, 50 µm. K, Representative images of macrophage migration assays and effects of conditioned medium from human LGALS3 + neutrophils on migration of macrophages (induced from THP-1 cells) in the presence of CCR1 inhibitor (BX471) or anti-CCL3 antibody ( n = 6). L, Comparison of immunosuppressive macrophage signature scores between colorectal cancer and CRLM. M, Schematic of the CRLM mouse model. C57BL/6 mice received intrasplenic injections of mouse colorectal cancer cells (MC38). Mice were subsequently treated with IgG control (IgG; n = 6), anti-Ly6G antibody (anti-Ly6G; n = 6), or anti-Ly6G plus anti-CD8a antibodies (anti-Ly6G + anti-CD8a; n = 6). Livers were harvested on day 14. N, Representative images of liver metastases from IgG, anti-Ly6G, and anti-Ly6G + anti-CD8a groups. O, Comparison of liver weights among the three groups. P values were calculated by the Wilcoxon rank-sum test ( B and L ) and unpaired Student t test ( F , K , and O ). *, P < 0.05; **, P < 0.01; ***, P < 0.001. CRC, colorectal cancer; Ctrl, control.
    Figure Legend Snippet: Proangiogenic and immunosuppression phenotype of TANs in the CRLM microenvironment. A, Heatmap showing signature scores for angiogenesis, myeloid cell recruitment, neutrophil cytotoxicity, MDSC, and NET across each TAN and PMN subset. B, Comparison of angiogenesis, myeloid cell recruitment, MDSC, and NET signature scores among TAN and PMN subsets. C, Dot plot illustrating expression levels of major cytokines and chemokines in each TAN and PMN subset. D, Representative IHC images of CD31 staining in CRLM tissues. Scale bars, 50 µm. E, Correlation analysis between CD31 and TAN1 density using Spearman’s rank correlation ( n = 102). F, Representative images and quantification of tube formation in HUVECs when cocultured with conditioned medium from human LGALS3 − neutrophils or LGALS3 + neutrophils ( n = 6). G, UMAP plot showing six monocyte/macrophage subsets across colorectal cancer, adjacent liver tissues, CRLM, and PB samples. H, Shell-like plot depicting ligand–receptor interaction strength between TAN1_LGASL3 and neutrophil/monocyte/macrophage subset in CRLM. I, Selected ligand–receptor interactions between TAN1_LGASL3 and neutrophil/monocyte/macrophage subset in CRLM. J, Representative mIHC images of CD68, CCL3L1, CD66b, CCR1, and BHLHE40 in CRLM. Scale bars, 50 µm. K, Representative images of macrophage migration assays and effects of conditioned medium from human LGALS3 + neutrophils on migration of macrophages (induced from THP-1 cells) in the presence of CCR1 inhibitor (BX471) or anti-CCL3 antibody ( n = 6). L, Comparison of immunosuppressive macrophage signature scores between colorectal cancer and CRLM. M, Schematic of the CRLM mouse model. C57BL/6 mice received intrasplenic injections of mouse colorectal cancer cells (MC38). Mice were subsequently treated with IgG control (IgG; n = 6), anti-Ly6G antibody (anti-Ly6G; n = 6), or anti-Ly6G plus anti-CD8a antibodies (anti-Ly6G + anti-CD8a; n = 6). Livers were harvested on day 14. N, Representative images of liver metastases from IgG, anti-Ly6G, and anti-Ly6G + anti-CD8a groups. O, Comparison of liver weights among the three groups. P values were calculated by the Wilcoxon rank-sum test ( B and L ) and unpaired Student t test ( F , K , and O ). *, P < 0.05; **, P < 0.01; ***, P < 0.001. CRC, colorectal cancer; Ctrl, control.

    Techniques Used: Comparison, Expressing, Staining, Analysis, Migration, Control

    Related Articles

    Control:

    Article Title: Syndecan-1 inhibition promotes antitumor immune response and facilitates the efficacy of anti-PD1 checkpoint immunotherapy.
    Article Snippet: Mouse IFN- γ was from PeproTech. .. InVivoMAb anti- mouse CD8a (BE0061), InVivoMAb rat IgG2b Isotype control (BE0090), InVivoMAb anti- mouse PD1 (BE0273), and InVivoMAb rat IgG2a Isotype control (BE0089) were obtained from BioXcell. ..

    Article Title: miR-22 gene therapy treats HCC by promoting anti-tumor immunity and enhancing metabolism
    Article Snippet: .. On the same day, HCCmice from each group were randomly divided into two groups to receive 200 mg of InVivoMAb anti-mouse CD8a (BE004-1, Bio X cell, Lebanon, NH, USA) or InVivoMAb rat IgG2a isotype control (BE0089, Bio X cell) via intraperitoneal injection twice per week for six times as indicated.75 IL-23 minicircle DNA production and hydrodynamic injection in HCC mice Minicircle (MC)-RSV.Flag.mIL23.elasti.bpA or RSV.eGFP.bpA was produced to induce IL17 signaling in HCC mice as described.76 Hydrodynamic delivery of 3 mg IL-23 or GFP MC DNA via tail vein injection was performed as previously described.77 At 1 week post oncogene injection, HCCmice were randomly assigned into AAV-miR-22 or AAV blank treated groups. ..


    In Vivo:

    Article Title: Steatohepatitis alters lymphocytes cytotoxicity and localization, accelerating colorectal liver metastases
    Article Snippet: .. Immune cell depletion experiments: In vivo depletion of CD8a + or CD4 + cells, was carried out prior to CRC cell intrasplenic injection, as follows: mice were injected i.p. with an initial dose of 200 μg/mouse of InVivoMAb anti-mouse CD8a, clone 2.43 or InVivoMab anti-mouse CD4, clone GK1.5 (Bio X Cell) followed by administration of 100 μg/mouse at intervals of three to four days until the mice were sacrificed. .. In both depletion experiments, control mice were injected with InVivoMab rat IgG2b isotype control, clone LTF-2 (Bio X Cell).

    Article Title: Steatohepatitis alters lymphocytes cytotoxicity and localization, accelerating colorectal liver metastases
    Article Snippet: .. Immune cell depletion experiments: In vivo depletion of CD8a+ or CD4+ cells, was carried out prior to CRC cell intrasplenic injection, as follows: mice were injected i.p. with an initial dose of 200 μg/mouse of InVivoMAb anti-mouse CD8a, clone 2.43 or InVivoMab anti-mouse CD4, clone GK1.5 (Bio X Cell) followed by administration of 100 μg/mouse at intervals of three to four days until the mice were sacrificed. .. In both depletion experiments, control mice were injected with InVivoMab rat IgG2b isotype control, clone LTF-2 (Bio X Cell).

    Injection:

    Article Title: Steatohepatitis alters lymphocytes cytotoxicity and localization, accelerating colorectal liver metastases
    Article Snippet: .. Immune cell depletion experiments: In vivo depletion of CD8a + or CD4 + cells, was carried out prior to CRC cell intrasplenic injection, as follows: mice were injected i.p. with an initial dose of 200 μg/mouse of InVivoMAb anti-mouse CD8a, clone 2.43 or InVivoMab anti-mouse CD4, clone GK1.5 (Bio X Cell) followed by administration of 100 μg/mouse at intervals of three to four days until the mice were sacrificed. .. In both depletion experiments, control mice were injected with InVivoMab rat IgG2b isotype control, clone LTF-2 (Bio X Cell).

    Article Title: miR-22 gene therapy treats HCC by promoting anti-tumor immunity and enhancing metabolism
    Article Snippet: .. On the same day, HCCmice from each group were randomly divided into two groups to receive 200 mg of InVivoMAb anti-mouse CD8a (BE004-1, Bio X cell, Lebanon, NH, USA) or InVivoMAb rat IgG2a isotype control (BE0089, Bio X cell) via intraperitoneal injection twice per week for six times as indicated.75 IL-23 minicircle DNA production and hydrodynamic injection in HCC mice Minicircle (MC)-RSV.Flag.mIL23.elasti.bpA or RSV.eGFP.bpA was produced to induce IL17 signaling in HCC mice as described.76 Hydrodynamic delivery of 3 mg IL-23 or GFP MC DNA via tail vein injection was performed as previously described.77 At 1 week post oncogene injection, HCCmice were randomly assigned into AAV-miR-22 or AAV blank treated groups. ..


    Article Title: Steatohepatitis alters lymphocytes cytotoxicity and localization, accelerating colorectal liver metastases
    Article Snippet: .. Immune cell depletion experiments: In vivo depletion of CD8a+ or CD4+ cells, was carried out prior to CRC cell intrasplenic injection, as follows: mice were injected i.p. with an initial dose of 200 μg/mouse of InVivoMAb anti-mouse CD8a, clone 2.43 or InVivoMab anti-mouse CD4, clone GK1.5 (Bio X Cell) followed by administration of 100 μg/mouse at intervals of three to four days until the mice were sacrificed. .. In both depletion experiments, control mice were injected with InVivoMab rat IgG2b isotype control, clone LTF-2 (Bio X Cell).

    Produced:

    Article Title: miR-22 gene therapy treats HCC by promoting anti-tumor immunity and enhancing metabolism
    Article Snippet: .. On the same day, HCCmice from each group were randomly divided into two groups to receive 200 mg of InVivoMAb anti-mouse CD8a (BE004-1, Bio X cell, Lebanon, NH, USA) or InVivoMAb rat IgG2a isotype control (BE0089, Bio X cell) via intraperitoneal injection twice per week for six times as indicated.75 IL-23 minicircle DNA production and hydrodynamic injection in HCC mice Minicircle (MC)-RSV.Flag.mIL23.elasti.bpA or RSV.eGFP.bpA was produced to induce IL17 signaling in HCC mice as described.76 Hydrodynamic delivery of 3 mg IL-23 or GFP MC DNA via tail vein injection was performed as previously described.77 At 1 week post oncogene injection, HCCmice were randomly assigned into AAV-miR-22 or AAV blank treated groups. ..

    Bioprocessing:

    Article Title: miR-22 gene therapy treats HCC by promoting anti-tumor immunity and enhancing metabolism
    Article Snippet: .. On the same day, HCCmice from each group were randomly divided into two groups to receive 200 mg of InVivoMAb anti-mouse CD8a (BE004-1, Bio X cell, Lebanon, NH, USA) or InVivoMAb rat IgG2a isotype control (BE0089, Bio X cell) via intraperitoneal injection twice per week for six times as indicated.75 IL-23 minicircle DNA production and hydrodynamic injection in HCC mice Minicircle (MC)-RSV.Flag.mIL23.elasti.bpA or RSV.eGFP.bpA was produced to induce IL17 signaling in HCC mice as described.76 Hydrodynamic delivery of 3 mg IL-23 or GFP MC DNA via tail vein injection was performed as previously described.77 At 1 week post oncogene injection, HCCmice were randomly assigned into AAV-miR-22 or AAV blank treated groups. ..



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    Proangiogenic and immunosuppression phenotype of TANs in the CRLM microenvironment. A, Heatmap showing signature scores for angiogenesis, myeloid cell recruitment, neutrophil cytotoxicity, MDSC, and NET across each TAN and PMN subset. B, Comparison of angiogenesis, myeloid cell recruitment, MDSC, and NET signature scores among TAN and PMN subsets. C, Dot plot illustrating expression levels of major cytokines and chemokines in each TAN and PMN subset. D, Representative IHC images of CD31 staining in CRLM tissues. Scale bars, 50 µm. E, Correlation analysis between CD31 and TAN1 density using Spearman’s rank correlation ( n = 102). F, Representative images and quantification of tube formation in HUVECs when cocultured with conditioned medium from human LGALS3 − neutrophils or LGALS3 + neutrophils ( n = 6). G, UMAP plot showing six monocyte/macrophage subsets across colorectal cancer, adjacent liver tissues, CRLM, and PB samples. H, Shell-like plot depicting ligand–receptor interaction strength between TAN1_LGASL3 and neutrophil/monocyte/macrophage subset in CRLM. I, Selected ligand–receptor interactions between TAN1_LGASL3 and neutrophil/monocyte/macrophage subset in CRLM. J, Representative mIHC images of CD68, CCL3L1, CD66b, CCR1, and BHLHE40 in CRLM. Scale bars, 50 µm. K, Representative images of macrophage migration assays and effects of conditioned medium from human LGALS3 + neutrophils on migration of macrophages (induced from THP-1 cells) in the presence of CCR1 inhibitor (BX471) or anti-CCL3 antibody ( n = 6). L, Comparison of immunosuppressive macrophage signature scores between colorectal cancer and CRLM. M, Schematic of the CRLM mouse model. C57BL/6 mice received intrasplenic injections of mouse colorectal cancer cells (MC38). Mice were subsequently treated with IgG control (IgG; n = 6), anti-Ly6G antibody (anti-Ly6G; n = 6), or anti-Ly6G plus <t>anti-CD8a</t> antibodies (anti-Ly6G + anti-CD8a; n = 6). Livers were harvested on day 14. N, Representative images of liver metastases from IgG, anti-Ly6G, and anti-Ly6G + anti-CD8a groups. O, Comparison of liver weights among the three groups. P values were calculated by the Wilcoxon rank-sum test ( B and L ) and unpaired Student t test ( F , K , and O ). *, P < 0.05; **, P < 0.01; ***, P < 0.001. CRC, colorectal cancer; Ctrl, control.
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    Proangiogenic and immunosuppression phenotype of TANs in the CRLM microenvironment. A, Heatmap showing signature scores for angiogenesis, myeloid cell recruitment, neutrophil cytotoxicity, MDSC, and NET across each TAN and PMN subset. B, Comparison of angiogenesis, myeloid cell recruitment, MDSC, and NET signature scores among TAN and PMN subsets. C, Dot plot illustrating expression levels of major cytokines and chemokines in each TAN and PMN subset. D, Representative IHC images of CD31 staining in CRLM tissues. Scale bars, 50 µm. E, Correlation analysis between CD31 and TAN1 density using Spearman’s rank correlation ( n = 102). F, Representative images and quantification of tube formation in HUVECs when cocultured with conditioned medium from human LGALS3 − neutrophils or LGALS3 + neutrophils ( n = 6). G, UMAP plot showing six monocyte/macrophage subsets across colorectal cancer, adjacent liver tissues, CRLM, and PB samples. H, Shell-like plot depicting ligand–receptor interaction strength between TAN1_LGASL3 and neutrophil/monocyte/macrophage subset in CRLM. I, Selected ligand–receptor interactions between TAN1_LGASL3 and neutrophil/monocyte/macrophage subset in CRLM. J, Representative mIHC images of CD68, CCL3L1, CD66b, CCR1, and BHLHE40 in CRLM. Scale bars, 50 µm. K, Representative images of macrophage migration assays and effects of conditioned medium from human LGALS3 + neutrophils on migration of macrophages (induced from THP-1 cells) in the presence of CCR1 inhibitor (BX471) or anti-CCL3 antibody ( n = 6). L, Comparison of immunosuppressive macrophage signature scores between colorectal cancer and CRLM. M, Schematic of the CRLM mouse model. C57BL/6 mice received intrasplenic injections of mouse colorectal cancer cells (MC38). Mice were subsequently treated with IgG control (IgG; n = 6), anti-Ly6G antibody (anti-Ly6G; n = 6), or anti-Ly6G plus anti-CD8a antibodies (anti-Ly6G + anti-CD8a; n = 6). Livers were harvested on day 14. N, Representative images of liver metastases from IgG, anti-Ly6G, and anti-Ly6G + anti-CD8a groups. O, Comparison of liver weights among the three groups. P values were calculated by the Wilcoxon rank-sum test ( B and L ) and unpaired Student t test ( F , K , and O ). *, P < 0.05; **, P < 0.01; ***, P < 0.001. CRC, colorectal cancer; Ctrl, control.

    Journal: Cancer Discovery

    Article Title: Senescent-Like Neutrophils Shape Angiogenic Immunosuppressive Niches in Colorectal Cancer Liver Metastasis

    doi: 10.1158/2159-8290.CD-25-0820

    Figure Lengend Snippet: Proangiogenic and immunosuppression phenotype of TANs in the CRLM microenvironment. A, Heatmap showing signature scores for angiogenesis, myeloid cell recruitment, neutrophil cytotoxicity, MDSC, and NET across each TAN and PMN subset. B, Comparison of angiogenesis, myeloid cell recruitment, MDSC, and NET signature scores among TAN and PMN subsets. C, Dot plot illustrating expression levels of major cytokines and chemokines in each TAN and PMN subset. D, Representative IHC images of CD31 staining in CRLM tissues. Scale bars, 50 µm. E, Correlation analysis between CD31 and TAN1 density using Spearman’s rank correlation ( n = 102). F, Representative images and quantification of tube formation in HUVECs when cocultured with conditioned medium from human LGALS3 − neutrophils or LGALS3 + neutrophils ( n = 6). G, UMAP plot showing six monocyte/macrophage subsets across colorectal cancer, adjacent liver tissues, CRLM, and PB samples. H, Shell-like plot depicting ligand–receptor interaction strength between TAN1_LGASL3 and neutrophil/monocyte/macrophage subset in CRLM. I, Selected ligand–receptor interactions between TAN1_LGASL3 and neutrophil/monocyte/macrophage subset in CRLM. J, Representative mIHC images of CD68, CCL3L1, CD66b, CCR1, and BHLHE40 in CRLM. Scale bars, 50 µm. K, Representative images of macrophage migration assays and effects of conditioned medium from human LGALS3 + neutrophils on migration of macrophages (induced from THP-1 cells) in the presence of CCR1 inhibitor (BX471) or anti-CCL3 antibody ( n = 6). L, Comparison of immunosuppressive macrophage signature scores between colorectal cancer and CRLM. M, Schematic of the CRLM mouse model. C57BL/6 mice received intrasplenic injections of mouse colorectal cancer cells (MC38). Mice were subsequently treated with IgG control (IgG; n = 6), anti-Ly6G antibody (anti-Ly6G; n = 6), or anti-Ly6G plus anti-CD8a antibodies (anti-Ly6G + anti-CD8a; n = 6). Livers were harvested on day 14. N, Representative images of liver metastases from IgG, anti-Ly6G, and anti-Ly6G + anti-CD8a groups. O, Comparison of liver weights among the three groups. P values were calculated by the Wilcoxon rank-sum test ( B and L ) and unpaired Student t test ( F , K , and O ). *, P < 0.05; **, P < 0.01; ***, P < 0.001. CRC, colorectal cancer; Ctrl, control.

    Article Snippet: For CD8 + T-cell depletion, 200 μg anti-mouse CD8a (Bio X Cell, BE0061, RRID: AB_1125541) was injected intraperitoneally twice a week.

    Techniques: Comparison, Expressing, Staining, Analysis, Migration, Control

    HDTVI-induced HCC-bearing mice received a single i.v. dose of 1 μg of DNA-LNP 3 weeks after HCC induction. Livers were harvested and analyzed at days 5 and 14 after treatment. ( A ) Cell-type profiling by NanoString. ( B ) qRT-PCR analysis of CD8a. ( C ) Representative images (20×) and ( D ) quantification of IHC analysis of CD8 + cells from liver sections. Min-to-max whiskers are shown in the box and whiskers plot. Data were analyzed by 1-way ANOVA with Tukey’s multiple-comparison test. * P < 0.05.

    Journal: JCI Insight

    Article Title: DNA delivered by lipid nanoparticles induces CD8 + T cell–dependent antitumor responses and enhances anti–PD-L1 therapy

    doi: 10.1172/jci.insight.197404

    Figure Lengend Snippet: HDTVI-induced HCC-bearing mice received a single i.v. dose of 1 μg of DNA-LNP 3 weeks after HCC induction. Livers were harvested and analyzed at days 5 and 14 after treatment. ( A ) Cell-type profiling by NanoString. ( B ) qRT-PCR analysis of CD8a. ( C ) Representative images (20×) and ( D ) quantification of IHC analysis of CD8 + cells from liver sections. Min-to-max whiskers are shown in the box and whiskers plot. Data were analyzed by 1-way ANOVA with Tukey’s multiple-comparison test. * P < 0.05.

    Article Snippet: In some experiments, anti-mouse CD8A antibodies (InVivoMAb, BE0061 clone 2.43, Bio X Cell) were i.p. administered on days –2, 1, 4, and 7 after DNA-LNP dosing at a dose of 200 μg/mouse in a total volume of 100 μL starting at day 1 after DNA-LNP dosing.

    Techniques: Quantitative RT-PCR, Comparison

    ( A – D ) B16-F10 tumor-bearing mice (s.c.) were intratumorally dosed with DNA-LNP at days 0 and 3. Tumors were collected at day 7 and analyzed using flow cytometry. ( A ) Numbers of indicated immune cells per milligram of tumor tissues. ( B ) CD4/CD8 ratio. ( C ) Percentage of Granzyme B + cells and ( D ) CD69 + cells from CD8 + T cells or NK cells. ( E and F ) Mice with B16-F10 lung metastasis were i.v. dosed at days 0, 3, and 6, and lung sections were analyzed at day 13 by CD8 IHC. ( E ) Representative images of lung sections and ( F ) quantification of CD8 + cells. Min-to-max whiskers are shown in the box and whiskers plot. Data shown as mean ± SD. Data were analyzed by 1-way ANOVA with Tukey’s multiple-comparison test. * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

    Journal: JCI Insight

    Article Title: DNA delivered by lipid nanoparticles induces CD8 + T cell–dependent antitumor responses and enhances anti–PD-L1 therapy

    doi: 10.1172/jci.insight.197404

    Figure Lengend Snippet: ( A – D ) B16-F10 tumor-bearing mice (s.c.) were intratumorally dosed with DNA-LNP at days 0 and 3. Tumors were collected at day 7 and analyzed using flow cytometry. ( A ) Numbers of indicated immune cells per milligram of tumor tissues. ( B ) CD4/CD8 ratio. ( C ) Percentage of Granzyme B + cells and ( D ) CD69 + cells from CD8 + T cells or NK cells. ( E and F ) Mice with B16-F10 lung metastasis were i.v. dosed at days 0, 3, and 6, and lung sections were analyzed at day 13 by CD8 IHC. ( E ) Representative images of lung sections and ( F ) quantification of CD8 + cells. Min-to-max whiskers are shown in the box and whiskers plot. Data shown as mean ± SD. Data were analyzed by 1-way ANOVA with Tukey’s multiple-comparison test. * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

    Article Snippet: In some experiments, anti-mouse CD8A antibodies (InVivoMAb, BE0061 clone 2.43, Bio X Cell) were i.p. administered on days –2, 1, 4, and 7 after DNA-LNP dosing at a dose of 200 μg/mouse in a total volume of 100 μL starting at day 1 after DNA-LNP dosing.

    Techniques: Flow Cytometry, Comparison

    HDTVI-induced HCC-bearing mice ( n = 11) received a single i.v. dose of 1 μg of DNA-LNP 3 weeks after HCC induction. Mice received 200 μg of anti-CD8 or anti-NK1.1 (i.p.) at days –2, 1, 4, and 7 to deplete CD8 + T cells or NK cells, respectively. ( A ) Tumor growth indicated by serum GLuc activity. ( B ) Survival curves. Survival data were analyzed by log-rank (Mantel-Cox) tests. * P < 0.05, *** P < 0.001, and ns (not significant).

    Journal: JCI Insight

    Article Title: DNA delivered by lipid nanoparticles induces CD8 + T cell–dependent antitumor responses and enhances anti–PD-L1 therapy

    doi: 10.1172/jci.insight.197404

    Figure Lengend Snippet: HDTVI-induced HCC-bearing mice ( n = 11) received a single i.v. dose of 1 μg of DNA-LNP 3 weeks after HCC induction. Mice received 200 μg of anti-CD8 or anti-NK1.1 (i.p.) at days –2, 1, 4, and 7 to deplete CD8 + T cells or NK cells, respectively. ( A ) Tumor growth indicated by serum GLuc activity. ( B ) Survival curves. Survival data were analyzed by log-rank (Mantel-Cox) tests. * P < 0.05, *** P < 0.001, and ns (not significant).

    Article Snippet: In some experiments, anti-mouse CD8A antibodies (InVivoMAb, BE0061 clone 2.43, Bio X Cell) were i.p. administered on days –2, 1, 4, and 7 after DNA-LNP dosing at a dose of 200 μg/mouse in a total volume of 100 μL starting at day 1 after DNA-LNP dosing.

    Techniques: Activity Assay

    Mouse tumor models received 200 μg of anti-CD8 or anti-NK1.1 (i.p.) at day –2, 1, 4, and 7 to deplete CD8 + T cells or NK cells, respectively. ( A ) Survival curves of C1498 AML tumor-bearing mice ( n = 8) after i.v. administration of 5 μg of DNA-LNP at days 0, 3, and 6. ( B ) Tumor growth curves and ( C ) survival curves of B16-F10 tumor-bearing mice ( n = 7) after intratumoral administration of 10 μg of DNA-LNP at days 0, 3, and 6. Survival data were analyzed by log-rank (Mantel-Cox) tests. * P < 0.05, ** P < 0.01, *** P < 0.001, and ns (not significant).

    Journal: JCI Insight

    Article Title: DNA delivered by lipid nanoparticles induces CD8 + T cell–dependent antitumor responses and enhances anti–PD-L1 therapy

    doi: 10.1172/jci.insight.197404

    Figure Lengend Snippet: Mouse tumor models received 200 μg of anti-CD8 or anti-NK1.1 (i.p.) at day –2, 1, 4, and 7 to deplete CD8 + T cells or NK cells, respectively. ( A ) Survival curves of C1498 AML tumor-bearing mice ( n = 8) after i.v. administration of 5 μg of DNA-LNP at days 0, 3, and 6. ( B ) Tumor growth curves and ( C ) survival curves of B16-F10 tumor-bearing mice ( n = 7) after intratumoral administration of 10 μg of DNA-LNP at days 0, 3, and 6. Survival data were analyzed by log-rank (Mantel-Cox) tests. * P < 0.05, ** P < 0.01, *** P < 0.001, and ns (not significant).

    Article Snippet: In some experiments, anti-mouse CD8A antibodies (InVivoMAb, BE0061 clone 2.43, Bio X Cell) were i.p. administered on days –2, 1, 4, and 7 after DNA-LNP dosing at a dose of 200 μg/mouse in a total volume of 100 μL starting at day 1 after DNA-LNP dosing.

    Techniques:

    ( A ) Schematic diagram of immune system activation. ( B ) Representative flow cytometric analysis and relative quantifications of mature DCs in tumor-draining lymph node cells after indicated treatment. ( C ) Analysis of B16F10 tumors after 21 days of treatment for effector cytokine production by intratumoral CD8 + T cells. Representative flow cytometric analysis images ( D ) and relative quantifications ( E ) of IFN-γ + CD8 + and GzmB + CD8 + T cells in the tumor. TILs, tumor-infiltrating lymphocytes. ( F and G ) Analysis of spleen in B16F10 tumor–bearing mice after 21 days of treatment for effector cytokine production by CD8 + T cells. ( H and I ) Analysis of spleen in B16F10 tumor–bearing mice after 21 days of treatment for effector cytokine production by NK + cells. ( J ) Analysis of B16F10 tumors after 21 days of treatment for effector cytokine production by intratumoral NK + cells. Representative flow cytometric analysis images ( K ) and relative quantifications ( L ) of IFN-γ + NK + and GzmB + NK + cells in the tumor. ( M to O ) Representative flow cytometric analysis and quantification of CD4 + CD25 + Foxp3 + cells in the tumor tissues and spleen. Results are presented as the means ± SD.

    Journal: Science Advances

    Article Title: PROTAC-based synthetic lethality strategy endogenously activates systemic STING to boost antitumor immunity

    doi: 10.1126/sciadv.ado7448

    Figure Lengend Snippet: ( A ) Schematic diagram of immune system activation. ( B ) Representative flow cytometric analysis and relative quantifications of mature DCs in tumor-draining lymph node cells after indicated treatment. ( C ) Analysis of B16F10 tumors after 21 days of treatment for effector cytokine production by intratumoral CD8 + T cells. Representative flow cytometric analysis images ( D ) and relative quantifications ( E ) of IFN-γ + CD8 + and GzmB + CD8 + T cells in the tumor. TILs, tumor-infiltrating lymphocytes. ( F and G ) Analysis of spleen in B16F10 tumor–bearing mice after 21 days of treatment for effector cytokine production by CD8 + T cells. ( H and I ) Analysis of spleen in B16F10 tumor–bearing mice after 21 days of treatment for effector cytokine production by NK + cells. ( J ) Analysis of B16F10 tumors after 21 days of treatment for effector cytokine production by intratumoral NK + cells. Representative flow cytometric analysis images ( K ) and relative quantifications ( L ) of IFN-γ + NK + and GzmB + NK + cells in the tumor. ( M to O ) Representative flow cytometric analysis and quantification of CD4 + CD25 + Foxp3 + cells in the tumor tissues and spleen. Results are presented as the means ± SD.

    Article Snippet: For the depletion of CD8 + T cells and NK1.1 cells in vivo, anti-CD8a antibodies (aCD8, 300 μg per mouse, BioXcell, catalog number BE0061, clone number 2.43) and anti-NK1.1 antibodies (aNK1.1, 300 μg per mouse, BioXcell, catalog number BE0036, clone number PK136) were intraperitoneally injected.

    Techniques: Activation Assay

    ( A ) Schematic illustration of the timeline for B16F10-Luc tumor inoculation and treatments in a C57BL/6 mouse model. ip, intraperitoneally. ( B ) In vivo bioluminescence imaging of B16F10-Luc tumor growth after administration with different formulations. n = 3 biologically independent samples. d, days. ( C ) Data analysis of the bioluminescence signals of the mice. Representative flow cytometry analysis plots of CD8 + T cells ( D ) and NK1.1 cells ( E ) in the spleens of mice after receiving LNP@PRO P+B and aCD8 + aNK1.1 + LNP@PRO P+B treatments. ( F ) Schematic diagram of the treatment process for the lung metastasis model. ( G ) Representative images of the excised lungs from each treatment group following the completion of the treatment. Yellow dashed lines indicate lung metastases. n = 5 biologically independent samples. ( H ) H&E-stained sections of the lungs of each treatment group after the end of treatment. ( I ) Statistics of the number of lung metastatic nodules in each treatment group after the end of treatment. ( J ) Weight of lung metastatic nodules in each treatment group after the end of treatment. ( K ) Representative flow cytometry analysis plots of CD8 + T cells and CD4 + T cells in the spleens of mice after receiving LNP@PRO P , LNP@PRO B , and LNP@PRO P+B treatments. ( L ) Quantitative analysis of the T EM cells and T CM cells in CD8 + T cells after the above treatments ( n = 5). ( M ) Representative flow cytometry analysis plots of T EM cells and T CM cells in CD8 + T cells after the above treatments. ( N ) Quantitative analysis of the T EM cells and T CM cells in CD4 + T cells after the above treatments ( n = 5). ( O ) Representative flow cytometry analysis plots of T EM and T CM cells in CD4 + T cells after the above treatments. Results are presented as the means ± SD.

    Journal: Science Advances

    Article Title: PROTAC-based synthetic lethality strategy endogenously activates systemic STING to boost antitumor immunity

    doi: 10.1126/sciadv.ado7448

    Figure Lengend Snippet: ( A ) Schematic illustration of the timeline for B16F10-Luc tumor inoculation and treatments in a C57BL/6 mouse model. ip, intraperitoneally. ( B ) In vivo bioluminescence imaging of B16F10-Luc tumor growth after administration with different formulations. n = 3 biologically independent samples. d, days. ( C ) Data analysis of the bioluminescence signals of the mice. Representative flow cytometry analysis plots of CD8 + T cells ( D ) and NK1.1 cells ( E ) in the spleens of mice after receiving LNP@PRO P+B and aCD8 + aNK1.1 + LNP@PRO P+B treatments. ( F ) Schematic diagram of the treatment process for the lung metastasis model. ( G ) Representative images of the excised lungs from each treatment group following the completion of the treatment. Yellow dashed lines indicate lung metastases. n = 5 biologically independent samples. ( H ) H&E-stained sections of the lungs of each treatment group after the end of treatment. ( I ) Statistics of the number of lung metastatic nodules in each treatment group after the end of treatment. ( J ) Weight of lung metastatic nodules in each treatment group after the end of treatment. ( K ) Representative flow cytometry analysis plots of CD8 + T cells and CD4 + T cells in the spleens of mice after receiving LNP@PRO P , LNP@PRO B , and LNP@PRO P+B treatments. ( L ) Quantitative analysis of the T EM cells and T CM cells in CD8 + T cells after the above treatments ( n = 5). ( M ) Representative flow cytometry analysis plots of T EM cells and T CM cells in CD8 + T cells after the above treatments. ( N ) Quantitative analysis of the T EM cells and T CM cells in CD4 + T cells after the above treatments ( n = 5). ( O ) Representative flow cytometry analysis plots of T EM and T CM cells in CD4 + T cells after the above treatments. Results are presented as the means ± SD.

    Article Snippet: For the depletion of CD8 + T cells and NK1.1 cells in vivo, anti-CD8a antibodies (aCD8, 300 μg per mouse, BioXcell, catalog number BE0061, clone number 2.43) and anti-NK1.1 antibodies (aNK1.1, 300 μg per mouse, BioXcell, catalog number BE0036, clone number PK136) were intraperitoneally injected.

    Techniques: In Vivo, Imaging, Flow Cytometry, Staining