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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 7965 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/b16f10+cells/B16-F10/pmc13122683-260-0-6
    Average 99 stars, based on 7965 article reviews
    b16f10 crl 6475 cells - by Bioz Stars, 2026-09
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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

    Related Articles

    Cell Culture:

    Article Title: Probing Immune Signatures of Conjugated Pattern Recognition Receptor Ligands Identifies Chimeras with Potent Adjuvant and Antitumor Activities.
    Article Snippet: .. B16F10 cells (ATCC: CRL-6475) were cultured in DMEM (4.5 g/L glucose) supplemented with 10% FBS, 100 U/mL penicillin, and 100 μg/mL streptomycin at 37 °C under a 5% CO2 atmosphere. ..

    Article Title: Targeting TMED4 enhances CD8 + T cell function and CAR T cell efficacy in solid tumors through the IRE1α-autophagy axis.
    Article Snippet: Cell culture and primary samples Jurkat cells were purchased from American Type Culture Collection (ATCC) and cultured in RPMI 1640 medium (BasalMedia, L210KJ) supplemented with 10% fetal bovine serum (FBS) and 1% penicillinstreptomycin (Gibco, 15140122). .. MC38 and B16F10 cells were obtained from ATCC and cultured in Dulbecco’s modified Eagle’s medium (DMEM) (BasalMedia, L110KJ) supplemented with 10% FBS and 1% penicillin- streptomycin (Gibco, 15140122). ..

    Article Title: DHHC3 interferes with antitumor immunity in melanoma cells.
    Article Snippet: CellRox and C12FDG kits were from Invitrogen. .. B16F10 cells were from ATCC and cultured in DMEM media (Invitrogen) containing 10% FBS (Sigma), HEPES and 1% penicillinstreptomycin (Invitrogen) at 37oC in humidified 5% CO2 incubator. .. Mycoplasma was tested using MycoAlert kit (Lonza Biologics).

    Article Title: A parametric study of mechanoporation through microfluidic design to modulate shear, compressive, and adhesion forces and loading rates
    Article Snippet: .. B16F10 cells were purchased from ATCC and cultured in DMEM (Gibco, Thermo Fisher Scientific, Waltham, MA) with 10% fetal bovine serum (FBS), 1% penicillin–streptomycin and 1% l -glutamine supplement as GlutaMAX (Gibco, Thermo Fisher Scientific, Waltham, MA). ..

    Article Title: Endogenous neoantigen-specific antibodies mediate antitumor responses and determine vaccine efficacy.
    Article Snippet: .. CT26 and B16F10 cells were obtained from American Type Culture Collection via the Duke Cell Culture Facility, and E0771 cells were purchased from CH3 Biosystems. ..

    Modification:

    Article Title: Targeting TMED4 enhances CD8 + T cell function and CAR T cell efficacy in solid tumors through the IRE1α-autophagy axis.
    Article Snippet: Cell culture and primary samples Jurkat cells were purchased from American Type Culture Collection (ATCC) and cultured in RPMI 1640 medium (BasalMedia, L210KJ) supplemented with 10% fetal bovine serum (FBS) and 1% penicillinstreptomycin (Gibco, 15140122). .. MC38 and B16F10 cells were obtained from ATCC and cultured in Dulbecco’s modified Eagle’s medium (DMEM) (BasalMedia, L110KJ) supplemented with 10% FBS and 1% penicillin- streptomycin (Gibco, 15140122). ..

    Article Title: Oncolytic virus-delivered GSDME: Unlocking pyroptosis to improve dendritic cell function and amplify cytotoxic T cell response
    Article Snippet: 597 EMT 6 cells were cultured in Waymouth’s MB752/1 (Gibco, #31220-023) supplemented with 15% 598 FBS (Gibco, #10100147). .. B16F10 cells (ATCC, CRL-6475) were maintained in Dulbecco’s 599 Modified Eagle’s Medium (DMEM; Gibco, #11960044) supplemented with 10% FCS (Gibco, 600 #10100147) and 2 mM CTS-GlutaMax-I (Gibco, #A1286001). ..



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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.
    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
    https://www.bioz.com/product/b16f10+cells/B16-F10/pm42258147-82-0-4
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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.
    Mouse B16f10 Melanoma 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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    pld2 ko b16f10 cell lines mouse b16f10 melanoma cells  (ATCC)
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    ATCC pld2 ko b16f10 cell lines mouse b16f10 melanoma 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.
    Pld2 Ko B16f10 Cell Lines Mouse B16f10 Melanoma 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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    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.
    Mouse 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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    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