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b16f10 crl 6475 cells  (ATCC)


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    ATCC b16f10 crl 6475 cells
    Dual protection against tumor and pathogen infection by the OV-BYTE strategy (A) Schematic of the experimental design for (B–D). C57BL/6 mice were infected with LCMV Armstrong and engrafted with MC38 cells on day 60 post-infection. On days 7–12 after tumor engraftment, recipients were daily administered PBS, NDV-WT, or NDV-GP daily via the intratumoral route. On day 15 after tumor engraftment, recipients were infected with either LM-GP 61-80 or IAV-GP 61-80 at an LD 50 dose. (B) Tumor growth curve of MC38 tumor-bearing mice intratumorally treated with PBS, NDV-WT, or NDV-GP as described in (A). (C and D) Survival curves of LM-GP 61-80 (C) and IAV-GP 61-80 (D) infection in MC38-engrafted mice treated with PBS, NDV-WT, or NDV-GP as described in (A). (E) Schematic of the experimental design for (F–H). C57BL/6 mice were infected with LCMV Armstrong and engrafted with <t>B16F10</t> cells on day 60 post-infection. On days 7–12 after tumor engraftment, recipients were administered PBS, Ad5-WT, or Ad5-GP daily via the intratumoral route. On day 15 after tumor engraftment, recipients were infected with either LM-GP 61-80 or IAV-GP 61-80 at an LD 50 dose. (F) Tumor growth curve of B16F10 tumor-bearing mice intratumorally treated with PBS, Ad5-WT, or Ad5-GP as described in (E). (G and H) Survival curves of LM-GP 61-80 (G) and IAV-GP 61-80 (H) infection in B16F10-engrafted mice treated with PBS, Ad5-WT, or Ad5-GP as described in (E). (I) Schematic of the experimental design. Congenic CD45.1 + SM CD4 + T cells were adoptively transferred into naive C57BL/6 recipients (CD45.2 + ), which were then infected with LCMV Armstrong. On day 60 post-infection, these recipients were engrafted with MC38 cells. On days 7–12, these recipients were administered NDV-GP daily via the intratumoral route. Then, Ly108 hi CD39 lo and Ly108 lo CD39 hi SM CD4 + T cells in the spleens were isolated on day 15 post-tumor engraftment and subsequently transferred into MC38 tumor-bearing mice (no LCMV Armstrong infection) via intravenous injection, along with MC38 tumor-bearing mice receiving no cell transfer as control. One day later, all recipients were infected with LM-GP 61-80 at an LD 50 dose. (J) Survival curve of LM-GP 61-80 infection in groups described in (I). (K) Schematic of the experimental design. WT and Gzmb KO mice were infected with LCMV Armstrong. On day 60 post-infection, splenic LCMV Armstrong-activated CD4 + T MEM cells were harvested and adoptively transferred into another cohort of naive C57BL/6 mice. These recipients, along with control C57BL/6 mice with no CD4 + T MEM cell transfer, were then engrafted with MC38 tumor cells, intratumorally administrated NDV-WT or NDV-GP, and infected with LM-GP 61-80 at the indicated time points. (L) Survival curve of LM-GP 61-80 infection in groups described in (I). All data are representative of at least two independent experiments with at least eight mice per group. Not significant (ns), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 by two-way ANOVA (B, F) and log rank (Mantel-Cox) test (C, D, G, H, J, L). Center values and error bars (B, F) indicate mean and SEM.
    B16f10 Crl 6475 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 7640 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/b16f10 crl 6475 cells/product/ATCC
    Average 99 stars, based on 7640 article reviews
    b16f10 crl 6475 cells - by Bioz Stars, 2026-06
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    Images

    1) Product Images from "Oncolytic virotherapy mobilizes tumor-resident, granzyme B-producing bystander CD4 + T cells to inhibit systemic microbial infection"

    Article Title: Oncolytic virotherapy mobilizes tumor-resident, granzyme B-producing bystander CD4 + T cells to inhibit systemic microbial infection

    Journal: Molecular Therapy Oncology

    doi: 10.1016/j.omton.2026.201187

    Dual protection against tumor and pathogen infection by the OV-BYTE strategy (A) Schematic of the experimental design for (B–D). C57BL/6 mice were infected with LCMV Armstrong and engrafted with MC38 cells on day 60 post-infection. On days 7–12 after tumor engraftment, recipients were daily administered PBS, NDV-WT, or NDV-GP daily via the intratumoral route. On day 15 after tumor engraftment, recipients were infected with either LM-GP 61-80 or IAV-GP 61-80 at an LD 50 dose. (B) Tumor growth curve of MC38 tumor-bearing mice intratumorally treated with PBS, NDV-WT, or NDV-GP as described in (A). (C and D) Survival curves of LM-GP 61-80 (C) and IAV-GP 61-80 (D) infection in MC38-engrafted mice treated with PBS, NDV-WT, or NDV-GP as described in (A). (E) Schematic of the experimental design for (F–H). C57BL/6 mice were infected with LCMV Armstrong and engrafted with B16F10 cells on day 60 post-infection. On days 7–12 after tumor engraftment, recipients were administered PBS, Ad5-WT, or Ad5-GP daily via the intratumoral route. On day 15 after tumor engraftment, recipients were infected with either LM-GP 61-80 or IAV-GP 61-80 at an LD 50 dose. (F) Tumor growth curve of B16F10 tumor-bearing mice intratumorally treated with PBS, Ad5-WT, or Ad5-GP as described in (E). (G and H) Survival curves of LM-GP 61-80 (G) and IAV-GP 61-80 (H) infection in B16F10-engrafted mice treated with PBS, Ad5-WT, or Ad5-GP as described in (E). (I) Schematic of the experimental design. Congenic CD45.1 + SM CD4 + T cells were adoptively transferred into naive C57BL/6 recipients (CD45.2 + ), which were then infected with LCMV Armstrong. On day 60 post-infection, these recipients were engrafted with MC38 cells. On days 7–12, these recipients were administered NDV-GP daily via the intratumoral route. Then, Ly108 hi CD39 lo and Ly108 lo CD39 hi SM CD4 + T cells in the spleens were isolated on day 15 post-tumor engraftment and subsequently transferred into MC38 tumor-bearing mice (no LCMV Armstrong infection) via intravenous injection, along with MC38 tumor-bearing mice receiving no cell transfer as control. One day later, all recipients were infected with LM-GP 61-80 at an LD 50 dose. (J) Survival curve of LM-GP 61-80 infection in groups described in (I). (K) Schematic of the experimental design. WT and Gzmb KO mice were infected with LCMV Armstrong. On day 60 post-infection, splenic LCMV Armstrong-activated CD4 + T MEM cells were harvested and adoptively transferred into another cohort of naive C57BL/6 mice. These recipients, along with control C57BL/6 mice with no CD4 + T MEM cell transfer, were then engrafted with MC38 tumor cells, intratumorally administrated NDV-WT or NDV-GP, and infected with LM-GP 61-80 at the indicated time points. (L) Survival curve of LM-GP 61-80 infection in groups described in (I). All data are representative of at least two independent experiments with at least eight mice per group. Not significant (ns), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 by two-way ANOVA (B, F) and log rank (Mantel-Cox) test (C, D, G, H, J, L). Center values and error bars (B, F) indicate mean and SEM.
    Figure Legend Snippet: Dual protection against tumor and pathogen infection by the OV-BYTE strategy (A) Schematic of the experimental design for (B–D). C57BL/6 mice were infected with LCMV Armstrong and engrafted with MC38 cells on day 60 post-infection. On days 7–12 after tumor engraftment, recipients were daily administered PBS, NDV-WT, or NDV-GP daily via the intratumoral route. On day 15 after tumor engraftment, recipients were infected with either LM-GP 61-80 or IAV-GP 61-80 at an LD 50 dose. (B) Tumor growth curve of MC38 tumor-bearing mice intratumorally treated with PBS, NDV-WT, or NDV-GP as described in (A). (C and D) Survival curves of LM-GP 61-80 (C) and IAV-GP 61-80 (D) infection in MC38-engrafted mice treated with PBS, NDV-WT, or NDV-GP as described in (A). (E) Schematic of the experimental design for (F–H). C57BL/6 mice were infected with LCMV Armstrong and engrafted with B16F10 cells on day 60 post-infection. On days 7–12 after tumor engraftment, recipients were administered PBS, Ad5-WT, or Ad5-GP daily via the intratumoral route. On day 15 after tumor engraftment, recipients were infected with either LM-GP 61-80 or IAV-GP 61-80 at an LD 50 dose. (F) Tumor growth curve of B16F10 tumor-bearing mice intratumorally treated with PBS, Ad5-WT, or Ad5-GP as described in (E). (G and H) Survival curves of LM-GP 61-80 (G) and IAV-GP 61-80 (H) infection in B16F10-engrafted mice treated with PBS, Ad5-WT, or Ad5-GP as described in (E). (I) Schematic of the experimental design. Congenic CD45.1 + SM CD4 + T cells were adoptively transferred into naive C57BL/6 recipients (CD45.2 + ), which were then infected with LCMV Armstrong. On day 60 post-infection, these recipients were engrafted with MC38 cells. On days 7–12, these recipients were administered NDV-GP daily via the intratumoral route. Then, Ly108 hi CD39 lo and Ly108 lo CD39 hi SM CD4 + T cells in the spleens were isolated on day 15 post-tumor engraftment and subsequently transferred into MC38 tumor-bearing mice (no LCMV Armstrong infection) via intravenous injection, along with MC38 tumor-bearing mice receiving no cell transfer as control. One day later, all recipients were infected with LM-GP 61-80 at an LD 50 dose. (J) Survival curve of LM-GP 61-80 infection in groups described in (I). (K) Schematic of the experimental design. WT and Gzmb KO mice were infected with LCMV Armstrong. On day 60 post-infection, splenic LCMV Armstrong-activated CD4 + T MEM cells were harvested and adoptively transferred into another cohort of naive C57BL/6 mice. These recipients, along with control C57BL/6 mice with no CD4 + T MEM cell transfer, were then engrafted with MC38 tumor cells, intratumorally administrated NDV-WT or NDV-GP, and infected with LM-GP 61-80 at the indicated time points. (L) Survival curve of LM-GP 61-80 infection in groups described in (I). All data are representative of at least two independent experiments with at least eight mice per group. Not significant (ns), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 by two-way ANOVA (B, F) and log rank (Mantel-Cox) test (C, D, G, H, J, L). Center values and error bars (B, F) indicate mean and SEM.

    Techniques Used: Infection, Isolation, Injection, Control



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    b16f10 crl 6475 cells  (ATCC)
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    ATCC b16f10 crl 6475 cells
    Dual protection against tumor and pathogen infection by the OV-BYTE strategy (A) Schematic of the experimental design for (B–D). C57BL/6 mice were infected with LCMV Armstrong and engrafted with MC38 cells on day 60 post-infection. On days 7–12 after tumor engraftment, recipients were daily administered PBS, NDV-WT, or NDV-GP daily via the intratumoral route. On day 15 after tumor engraftment, recipients were infected with either LM-GP 61-80 or IAV-GP 61-80 at an LD 50 dose. (B) Tumor growth curve of MC38 tumor-bearing mice intratumorally treated with PBS, NDV-WT, or NDV-GP as described in (A). (C and D) Survival curves of LM-GP 61-80 (C) and IAV-GP 61-80 (D) infection in MC38-engrafted mice treated with PBS, NDV-WT, or NDV-GP as described in (A). (E) Schematic of the experimental design for (F–H). C57BL/6 mice were infected with LCMV Armstrong and engrafted with <t>B16F10</t> cells on day 60 post-infection. On days 7–12 after tumor engraftment, recipients were administered PBS, Ad5-WT, or Ad5-GP daily via the intratumoral route. On day 15 after tumor engraftment, recipients were infected with either LM-GP 61-80 or IAV-GP 61-80 at an LD 50 dose. (F) Tumor growth curve of B16F10 tumor-bearing mice intratumorally treated with PBS, Ad5-WT, or Ad5-GP as described in (E). (G and H) Survival curves of LM-GP 61-80 (G) and IAV-GP 61-80 (H) infection in B16F10-engrafted mice treated with PBS, Ad5-WT, or Ad5-GP as described in (E). (I) Schematic of the experimental design. Congenic CD45.1 + SM CD4 + T cells were adoptively transferred into naive C57BL/6 recipients (CD45.2 + ), which were then infected with LCMV Armstrong. On day 60 post-infection, these recipients were engrafted with MC38 cells. On days 7–12, these recipients were administered NDV-GP daily via the intratumoral route. Then, Ly108 hi CD39 lo and Ly108 lo CD39 hi SM CD4 + T cells in the spleens were isolated on day 15 post-tumor engraftment and subsequently transferred into MC38 tumor-bearing mice (no LCMV Armstrong infection) via intravenous injection, along with MC38 tumor-bearing mice receiving no cell transfer as control. One day later, all recipients were infected with LM-GP 61-80 at an LD 50 dose. (J) Survival curve of LM-GP 61-80 infection in groups described in (I). (K) Schematic of the experimental design. WT and Gzmb KO mice were infected with LCMV Armstrong. On day 60 post-infection, splenic LCMV Armstrong-activated CD4 + T MEM cells were harvested and adoptively transferred into another cohort of naive C57BL/6 mice. These recipients, along with control C57BL/6 mice with no CD4 + T MEM cell transfer, were then engrafted with MC38 tumor cells, intratumorally administrated NDV-WT or NDV-GP, and infected with LM-GP 61-80 at the indicated time points. (L) Survival curve of LM-GP 61-80 infection in groups described in (I). All data are representative of at least two independent experiments with at least eight mice per group. Not significant (ns), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 by two-way ANOVA (B, F) and log rank (Mantel-Cox) test (C, D, G, H, J, L). Center values and error bars (B, F) indicate mean and SEM.
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    Dual protection against tumor and pathogen infection by the OV-BYTE strategy (A) Schematic of the experimental design for (B–D). C57BL/6 mice were infected with LCMV Armstrong and engrafted with MC38 cells on day 60 post-infection. On days 7–12 after tumor engraftment, recipients were daily administered PBS, NDV-WT, or NDV-GP daily via the intratumoral route. On day 15 after tumor engraftment, recipients were infected with either LM-GP 61-80 or IAV-GP 61-80 at an LD 50 dose. (B) Tumor growth curve of MC38 tumor-bearing mice intratumorally treated with PBS, NDV-WT, or NDV-GP as described in (A). (C and D) Survival curves of LM-GP 61-80 (C) and IAV-GP 61-80 (D) infection in MC38-engrafted mice treated with PBS, NDV-WT, or NDV-GP as described in (A). (E) Schematic of the experimental design for (F–H). C57BL/6 mice were infected with LCMV Armstrong and engrafted with <t>B16F10</t> cells on day 60 post-infection. On days 7–12 after tumor engraftment, recipients were administered PBS, Ad5-WT, or Ad5-GP daily via the intratumoral route. On day 15 after tumor engraftment, recipients were infected with either LM-GP 61-80 or IAV-GP 61-80 at an LD 50 dose. (F) Tumor growth curve of B16F10 tumor-bearing mice intratumorally treated with PBS, Ad5-WT, or Ad5-GP as described in (E). (G and H) Survival curves of LM-GP 61-80 (G) and IAV-GP 61-80 (H) infection in B16F10-engrafted mice treated with PBS, Ad5-WT, or Ad5-GP as described in (E). (I) Schematic of the experimental design. Congenic CD45.1 + SM CD4 + T cells were adoptively transferred into naive C57BL/6 recipients (CD45.2 + ), which were then infected with LCMV Armstrong. On day 60 post-infection, these recipients were engrafted with MC38 cells. On days 7–12, these recipients were administered NDV-GP daily via the intratumoral route. Then, Ly108 hi CD39 lo and Ly108 lo CD39 hi SM CD4 + T cells in the spleens were isolated on day 15 post-tumor engraftment and subsequently transferred into MC38 tumor-bearing mice (no LCMV Armstrong infection) via intravenous injection, along with MC38 tumor-bearing mice receiving no cell transfer as control. One day later, all recipients were infected with LM-GP 61-80 at an LD 50 dose. (J) Survival curve of LM-GP 61-80 infection in groups described in (I). (K) Schematic of the experimental design. WT and Gzmb KO mice were infected with LCMV Armstrong. On day 60 post-infection, splenic LCMV Armstrong-activated CD4 + T MEM cells were harvested and adoptively transferred into another cohort of naive C57BL/6 mice. These recipients, along with control C57BL/6 mice with no CD4 + T MEM cell transfer, were then engrafted with MC38 tumor cells, intratumorally administrated NDV-WT or NDV-GP, and infected with LM-GP 61-80 at the indicated time points. (L) Survival curve of LM-GP 61-80 infection in groups described in (I). All data are representative of at least two independent experiments with at least eight mice per group. Not significant (ns), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 by two-way ANOVA (B, F) and log rank (Mantel-Cox) test (C, D, G, H, J, L). Center values and error bars (B, F) indicate mean and SEM.
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    Dual protection against tumor and pathogen infection by the OV-BYTE strategy (A) Schematic of the experimental design for (B–D). C57BL/6 mice were infected with LCMV Armstrong and engrafted with MC38 cells on day 60 post-infection. On days 7–12 after tumor engraftment, recipients were daily administered PBS, NDV-WT, or NDV-GP daily via the intratumoral route. On day 15 after tumor engraftment, recipients were infected with either LM-GP 61-80 or IAV-GP 61-80 at an LD 50 dose. (B) Tumor growth curve of MC38 tumor-bearing mice intratumorally treated with PBS, NDV-WT, or NDV-GP as described in (A). (C and D) Survival curves of LM-GP 61-80 (C) and IAV-GP 61-80 (D) infection in MC38-engrafted mice treated with PBS, NDV-WT, or NDV-GP as described in (A). (E) Schematic of the experimental design for (F–H). C57BL/6 mice were infected with LCMV Armstrong and engrafted with <t>B16F10</t> cells on day 60 post-infection. On days 7–12 after tumor engraftment, recipients were administered PBS, Ad5-WT, or Ad5-GP daily via the intratumoral route. On day 15 after tumor engraftment, recipients were infected with either LM-GP 61-80 or IAV-GP 61-80 at an LD 50 dose. (F) Tumor growth curve of B16F10 tumor-bearing mice intratumorally treated with PBS, Ad5-WT, or Ad5-GP as described in (E). (G and H) Survival curves of LM-GP 61-80 (G) and IAV-GP 61-80 (H) infection in B16F10-engrafted mice treated with PBS, Ad5-WT, or Ad5-GP as described in (E). (I) Schematic of the experimental design. Congenic CD45.1 + SM CD4 + T cells were adoptively transferred into naive C57BL/6 recipients (CD45.2 + ), which were then infected with LCMV Armstrong. On day 60 post-infection, these recipients were engrafted with MC38 cells. On days 7–12, these recipients were administered NDV-GP daily via the intratumoral route. Then, Ly108 hi CD39 lo and Ly108 lo CD39 hi SM CD4 + T cells in the spleens were isolated on day 15 post-tumor engraftment and subsequently transferred into MC38 tumor-bearing mice (no LCMV Armstrong infection) via intravenous injection, along with MC38 tumor-bearing mice receiving no cell transfer as control. One day later, all recipients were infected with LM-GP 61-80 at an LD 50 dose. (J) Survival curve of LM-GP 61-80 infection in groups described in (I). (K) Schematic of the experimental design. WT and Gzmb KO mice were infected with LCMV Armstrong. On day 60 post-infection, splenic LCMV Armstrong-activated CD4 + T MEM cells were harvested and adoptively transferred into another cohort of naive C57BL/6 mice. These recipients, along with control C57BL/6 mice with no CD4 + T MEM cell transfer, were then engrafted with MC38 tumor cells, intratumorally administrated NDV-WT or NDV-GP, and infected with LM-GP 61-80 at the indicated time points. (L) Survival curve of LM-GP 61-80 infection in groups described in (I). All data are representative of at least two independent experiments with at least eight mice per group. Not significant (ns), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 by two-way ANOVA (B, F) and log rank (Mantel-Cox) test (C, D, G, H, J, L). Center values and error bars (B, F) indicate mean and SEM.
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    ATCC murine melanoma cell line b16f10
    Dual protection against tumor and pathogen infection by the OV-BYTE strategy (A) Schematic of the experimental design for (B–D). C57BL/6 mice were infected with LCMV Armstrong and engrafted with MC38 cells on day 60 post-infection. On days 7–12 after tumor engraftment, recipients were daily administered PBS, NDV-WT, or NDV-GP daily via the intratumoral route. On day 15 after tumor engraftment, recipients were infected with either LM-GP 61-80 or IAV-GP 61-80 at an LD 50 dose. (B) Tumor growth curve of MC38 tumor-bearing mice intratumorally treated with PBS, NDV-WT, or NDV-GP as described in (A). (C and D) Survival curves of LM-GP 61-80 (C) and IAV-GP 61-80 (D) infection in MC38-engrafted mice treated with PBS, NDV-WT, or NDV-GP as described in (A). (E) Schematic of the experimental design for (F–H). C57BL/6 mice were infected with LCMV Armstrong and engrafted with <t>B16F10</t> cells on day 60 post-infection. On days 7–12 after tumor engraftment, recipients were administered PBS, Ad5-WT, or Ad5-GP daily via the intratumoral route. On day 15 after tumor engraftment, recipients were infected with either LM-GP 61-80 or IAV-GP 61-80 at an LD 50 dose. (F) Tumor growth curve of B16F10 tumor-bearing mice intratumorally treated with PBS, Ad5-WT, or Ad5-GP as described in (E). (G and H) Survival curves of LM-GP 61-80 (G) and IAV-GP 61-80 (H) infection in B16F10-engrafted mice treated with PBS, Ad5-WT, or Ad5-GP as described in (E). (I) Schematic of the experimental design. Congenic CD45.1 + SM CD4 + T cells were adoptively transferred into naive C57BL/6 recipients (CD45.2 + ), which were then infected with LCMV Armstrong. On day 60 post-infection, these recipients were engrafted with MC38 cells. On days 7–12, these recipients were administered NDV-GP daily via the intratumoral route. Then, Ly108 hi CD39 lo and Ly108 lo CD39 hi SM CD4 + T cells in the spleens were isolated on day 15 post-tumor engraftment and subsequently transferred into MC38 tumor-bearing mice (no LCMV Armstrong infection) via intravenous injection, along with MC38 tumor-bearing mice receiving no cell transfer as control. One day later, all recipients were infected with LM-GP 61-80 at an LD 50 dose. (J) Survival curve of LM-GP 61-80 infection in groups described in (I). (K) Schematic of the experimental design. WT and Gzmb KO mice were infected with LCMV Armstrong. On day 60 post-infection, splenic LCMV Armstrong-activated CD4 + T MEM cells were harvested and adoptively transferred into another cohort of naive C57BL/6 mice. These recipients, along with control C57BL/6 mice with no CD4 + T MEM cell transfer, were then engrafted with MC38 tumor cells, intratumorally administrated NDV-WT or NDV-GP, and infected with LM-GP 61-80 at the indicated time points. (L) Survival curve of LM-GP 61-80 infection in groups described in (I). All data are representative of at least two independent experiments with at least eight mice per group. Not significant (ns), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 by two-way ANOVA (B, F) and log rank (Mantel-Cox) test (C, D, G, H, J, L). Center values and error bars (B, F) indicate mean and SEM.
    Murine Melanoma Cell Line B16f10, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    b16f10 murine melanoma cell line  (ATCC)
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    ATCC b16f10 murine melanoma cell line
    (A) Schematic illustrating the generation of CD8-specific ME1 transgenic (ME1 Tg) mice. (B) Representative flow cytometry showing tdTomato expression as a surrogate for ME1 overexpression in CD8 + tumor-infiltrating lymphocytes (TILs). (C–D) Average growth curves of <t>B16F10</t> tumors in control and CD8-ME1 Tg mice treated with PBS (C) or combined anti-PD-1/anti-PD-L1 antibodies (100 μg each per dose) administered every other day starting on day 6 (arrow) after tumor implantation. Tumor growth was analyzed by two-way ANOVA (D, n = 6, **P < 0.01). (E) Tumor sizes were measured at endpoint. Data were analyzed using an unpaired two-tailed t test (n = 4–8, ***P < 0.001). One of two independent experiments is shown. (F) Flow cytometric analysis of granzyme B (GZMB) protein expression in CD8 + TILs cells from B16F10 tumors in ME1 Tg and control mice on day 12. Data were analyzed using an unpaired two-tailed Student’s t test ( * P< 0.05; n = 5 mice per group).
    B16f10 Murine Melanoma Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    b16f10 flt3l  (ATCC)
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    ATCC b16f10 flt3l
    (A) Schematic illustrating the generation of CD8-specific ME1 transgenic (ME1 Tg) mice. (B) Representative flow cytometry showing tdTomato expression as a surrogate for ME1 overexpression in CD8 + tumor-infiltrating lymphocytes (TILs). (C–D) Average growth curves of <t>B16F10</t> tumors in control and CD8-ME1 Tg mice treated with PBS (C) or combined anti-PD-1/anti-PD-L1 antibodies (100 μg each per dose) administered every other day starting on day 6 (arrow) after tumor implantation. Tumor growth was analyzed by two-way ANOVA (D, n = 6, **P < 0.01). (E) Tumor sizes were measured at endpoint. Data were analyzed using an unpaired two-tailed t test (n = 4–8, ***P < 0.001). One of two independent experiments is shown. (F) Flow cytometric analysis of granzyme B (GZMB) protein expression in CD8 + TILs cells from B16F10 tumors in ME1 Tg and control mice on day 12. Data were analyzed using an unpaired two-tailed Student’s t test ( * P< 0.05; n = 5 mice per group).
    B16f10 Flt3l, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    b16f10 cells  (ATCC)
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    ATCC b16f10 cells
    (A) Schematic illustrating the generation of CD8-specific ME1 transgenic (ME1 Tg) mice. (B) Representative flow cytometry showing tdTomato expression as a surrogate for ME1 overexpression in CD8 + tumor-infiltrating lymphocytes (TILs). (C–D) Average growth curves of <t>B16F10</t> tumors in control and CD8-ME1 Tg mice treated with PBS (C) or combined anti-PD-1/anti-PD-L1 antibodies (100 μg each per dose) administered every other day starting on day 6 (arrow) after tumor implantation. Tumor growth was analyzed by two-way ANOVA (D, n = 6, **P < 0.01). (E) Tumor sizes were measured at endpoint. Data were analyzed using an unpaired two-tailed t test (n = 4–8, ***P < 0.001). One of two independent experiments is shown. (F) Flow cytometric analysis of granzyme B (GZMB) protein expression in CD8 + TILs cells from B16F10 tumors in ME1 Tg and control mice on day 12. Data were analyzed using an unpaired two-tailed Student’s t test ( * P< 0.05; n = 5 mice per group).
    B16f10 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    murine melanoma b16f10  (ATCC)
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    ATCC murine melanoma b16f10
    (A) Schematic illustrating the generation of CD8-specific ME1 transgenic (ME1 Tg) mice. (B) Representative flow cytometry showing tdTomato expression as a surrogate for ME1 overexpression in CD8 + tumor-infiltrating lymphocytes (TILs). (C–D) Average growth curves of <t>B16F10</t> tumors in control and CD8-ME1 Tg mice treated with PBS (C) or combined anti-PD-1/anti-PD-L1 antibodies (100 μg each per dose) administered every other day starting on day 6 (arrow) after tumor implantation. Tumor growth was analyzed by two-way ANOVA (D, n = 6, **P < 0.01). (E) Tumor sizes were measured at endpoint. Data were analyzed using an unpaired two-tailed t test (n = 4–8, ***P < 0.001). One of two independent experiments is shown. (F) Flow cytometric analysis of granzyme B (GZMB) protein expression in CD8 + TILs cells from B16F10 tumors in ME1 Tg and control mice on day 12. Data were analyzed using an unpaired two-tailed Student’s t test ( * P< 0.05; n = 5 mice per group).
    Murine Melanoma B16f10, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Dual protection against tumor and pathogen infection by the OV-BYTE strategy (A) Schematic of the experimental design for (B–D). C57BL/6 mice were infected with LCMV Armstrong and engrafted with MC38 cells on day 60 post-infection. On days 7–12 after tumor engraftment, recipients were daily administered PBS, NDV-WT, or NDV-GP daily via the intratumoral route. On day 15 after tumor engraftment, recipients were infected with either LM-GP 61-80 or IAV-GP 61-80 at an LD 50 dose. (B) Tumor growth curve of MC38 tumor-bearing mice intratumorally treated with PBS, NDV-WT, or NDV-GP as described in (A). (C and D) Survival curves of LM-GP 61-80 (C) and IAV-GP 61-80 (D) infection in MC38-engrafted mice treated with PBS, NDV-WT, or NDV-GP as described in (A). (E) Schematic of the experimental design for (F–H). C57BL/6 mice were infected with LCMV Armstrong and engrafted with B16F10 cells on day 60 post-infection. On days 7–12 after tumor engraftment, recipients were administered PBS, Ad5-WT, or Ad5-GP daily via the intratumoral route. On day 15 after tumor engraftment, recipients were infected with either LM-GP 61-80 or IAV-GP 61-80 at an LD 50 dose. (F) Tumor growth curve of B16F10 tumor-bearing mice intratumorally treated with PBS, Ad5-WT, or Ad5-GP as described in (E). (G and H) Survival curves of LM-GP 61-80 (G) and IAV-GP 61-80 (H) infection in B16F10-engrafted mice treated with PBS, Ad5-WT, or Ad5-GP as described in (E). (I) Schematic of the experimental design. Congenic CD45.1 + SM CD4 + T cells were adoptively transferred into naive C57BL/6 recipients (CD45.2 + ), which were then infected with LCMV Armstrong. On day 60 post-infection, these recipients were engrafted with MC38 cells. On days 7–12, these recipients were administered NDV-GP daily via the intratumoral route. Then, Ly108 hi CD39 lo and Ly108 lo CD39 hi SM CD4 + T cells in the spleens were isolated on day 15 post-tumor engraftment and subsequently transferred into MC38 tumor-bearing mice (no LCMV Armstrong infection) via intravenous injection, along with MC38 tumor-bearing mice receiving no cell transfer as control. One day later, all recipients were infected with LM-GP 61-80 at an LD 50 dose. (J) Survival curve of LM-GP 61-80 infection in groups described in (I). (K) Schematic of the experimental design. WT and Gzmb KO mice were infected with LCMV Armstrong. On day 60 post-infection, splenic LCMV Armstrong-activated CD4 + T MEM cells were harvested and adoptively transferred into another cohort of naive C57BL/6 mice. These recipients, along with control C57BL/6 mice with no CD4 + T MEM cell transfer, were then engrafted with MC38 tumor cells, intratumorally administrated NDV-WT or NDV-GP, and infected with LM-GP 61-80 at the indicated time points. (L) Survival curve of LM-GP 61-80 infection in groups described in (I). All data are representative of at least two independent experiments with at least eight mice per group. Not significant (ns), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 by two-way ANOVA (B, F) and log rank (Mantel-Cox) test (C, D, G, H, J, L). Center values and error bars (B, F) indicate mean and SEM.

    Journal: Molecular Therapy Oncology

    Article Title: Oncolytic virotherapy mobilizes tumor-resident, granzyme B-producing bystander CD4 + T cells to inhibit systemic microbial infection

    doi: 10.1016/j.omton.2026.201187

    Figure Lengend Snippet: Dual protection against tumor and pathogen infection by the OV-BYTE strategy (A) Schematic of the experimental design for (B–D). C57BL/6 mice were infected with LCMV Armstrong and engrafted with MC38 cells on day 60 post-infection. On days 7–12 after tumor engraftment, recipients were daily administered PBS, NDV-WT, or NDV-GP daily via the intratumoral route. On day 15 after tumor engraftment, recipients were infected with either LM-GP 61-80 or IAV-GP 61-80 at an LD 50 dose. (B) Tumor growth curve of MC38 tumor-bearing mice intratumorally treated with PBS, NDV-WT, or NDV-GP as described in (A). (C and D) Survival curves of LM-GP 61-80 (C) and IAV-GP 61-80 (D) infection in MC38-engrafted mice treated with PBS, NDV-WT, or NDV-GP as described in (A). (E) Schematic of the experimental design for (F–H). C57BL/6 mice were infected with LCMV Armstrong and engrafted with B16F10 cells on day 60 post-infection. On days 7–12 after tumor engraftment, recipients were administered PBS, Ad5-WT, or Ad5-GP daily via the intratumoral route. On day 15 after tumor engraftment, recipients were infected with either LM-GP 61-80 or IAV-GP 61-80 at an LD 50 dose. (F) Tumor growth curve of B16F10 tumor-bearing mice intratumorally treated with PBS, Ad5-WT, or Ad5-GP as described in (E). (G and H) Survival curves of LM-GP 61-80 (G) and IAV-GP 61-80 (H) infection in B16F10-engrafted mice treated with PBS, Ad5-WT, or Ad5-GP as described in (E). (I) Schematic of the experimental design. Congenic CD45.1 + SM CD4 + T cells were adoptively transferred into naive C57BL/6 recipients (CD45.2 + ), which were then infected with LCMV Armstrong. On day 60 post-infection, these recipients were engrafted with MC38 cells. On days 7–12, these recipients were administered NDV-GP daily via the intratumoral route. Then, Ly108 hi CD39 lo and Ly108 lo CD39 hi SM CD4 + T cells in the spleens were isolated on day 15 post-tumor engraftment and subsequently transferred into MC38 tumor-bearing mice (no LCMV Armstrong infection) via intravenous injection, along with MC38 tumor-bearing mice receiving no cell transfer as control. One day later, all recipients were infected with LM-GP 61-80 at an LD 50 dose. (J) Survival curve of LM-GP 61-80 infection in groups described in (I). (K) Schematic of the experimental design. WT and Gzmb KO mice were infected with LCMV Armstrong. On day 60 post-infection, splenic LCMV Armstrong-activated CD4 + T MEM cells were harvested and adoptively transferred into another cohort of naive C57BL/6 mice. These recipients, along with control C57BL/6 mice with no CD4 + T MEM cell transfer, were then engrafted with MC38 tumor cells, intratumorally administrated NDV-WT or NDV-GP, and infected with LM-GP 61-80 at the indicated time points. (L) Survival curve of LM-GP 61-80 infection in groups described in (I). All data are representative of at least two independent experiments with at least eight mice per group. Not significant (ns), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 by two-way ANOVA (B, F) and log rank (Mantel-Cox) test (C, D, G, H, J, L). Center values and error bars (B, F) indicate mean and SEM.

    Article Snippet: B16F10 (CRL-6475) cells were acquired from ATCC.

    Techniques: Infection, Isolation, Injection, Control

    (A) Schematic illustrating the generation of CD8-specific ME1 transgenic (ME1 Tg) mice. (B) Representative flow cytometry showing tdTomato expression as a surrogate for ME1 overexpression in CD8 + tumor-infiltrating lymphocytes (TILs). (C–D) Average growth curves of B16F10 tumors in control and CD8-ME1 Tg mice treated with PBS (C) or combined anti-PD-1/anti-PD-L1 antibodies (100 μg each per dose) administered every other day starting on day 6 (arrow) after tumor implantation. Tumor growth was analyzed by two-way ANOVA (D, n = 6, **P < 0.01). (E) Tumor sizes were measured at endpoint. Data were analyzed using an unpaired two-tailed t test (n = 4–8, ***P < 0.001). One of two independent experiments is shown. (F) Flow cytometric analysis of granzyme B (GZMB) protein expression in CD8 + TILs cells from B16F10 tumors in ME1 Tg and control mice on day 12. Data were analyzed using an unpaired two-tailed Student’s t test ( * P< 0.05; n = 5 mice per group).

    Journal: bioRxiv

    Article Title: ME1 Programs Latent Effector Capacity and Grounds a Mathematical Model of Reversible T Cell Exhaustion

    doi: 10.64898/2026.05.05.722814

    Figure Lengend Snippet: (A) Schematic illustrating the generation of CD8-specific ME1 transgenic (ME1 Tg) mice. (B) Representative flow cytometry showing tdTomato expression as a surrogate for ME1 overexpression in CD8 + tumor-infiltrating lymphocytes (TILs). (C–D) Average growth curves of B16F10 tumors in control and CD8-ME1 Tg mice treated with PBS (C) or combined anti-PD-1/anti-PD-L1 antibodies (100 μg each per dose) administered every other day starting on day 6 (arrow) after tumor implantation. Tumor growth was analyzed by two-way ANOVA (D, n = 6, **P < 0.01). (E) Tumor sizes were measured at endpoint. Data were analyzed using an unpaired two-tailed t test (n = 4–8, ***P < 0.001). One of two independent experiments is shown. (F) Flow cytometric analysis of granzyme B (GZMB) protein expression in CD8 + TILs cells from B16F10 tumors in ME1 Tg and control mice on day 12. Data were analyzed using an unpaired two-tailed Student’s t test ( * P< 0.05; n = 5 mice per group).

    Article Snippet: B16F10 murine melanoma cell line was purchased from ATCC (CRL-6475) and cultured using DMEM complete medium.

    Techniques: Transgenic Assay, Flow Cytometry, Expressing, Over Expression, Control, Tumor Implantation, Two Tailed Test