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l1210 mouse cell lines  (ATCC)


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    Structured Review

    ATCC l1210 mouse cell lines
    Pola‐induced infiltration of MΦs and NK cells contributes to the antitumor effect of Pola in the <t>L1210‐hCD79b‐9</t> syngeneic mouse model. (A) Sensitivity of L1210 and L1210‐hCD79b‐9 cells to Pola at the indicated concentrations (3 replicates). The data represent the mean + SD. (B) Percentage of the area of CD68‐positive staining cells to the total area of tumor cells and (C) percentage of NCR1‐positive cells among tumor cells after 4 mg/kg ctrl IgG or 4 mg/kg Pola administration in the L1210‐hCD79b‐9 syngeneic mouse model ( n = 8). * p < 0.05 by Student's t ‐test. In dot plots, horizontal bars represent median values. (D) L1210‐hCD79b‐9 tumor growth curves from Day 0 to Day 9 after administration of 4 mg/kg ctrl IgG, 4 mg/kg Pola, or 4 mg/kg Pola plus clodronate liposomes plus anti‐asialo GM1 ( n = 6–7). (E) Numbers of mice presenting L1210‐hCD79b‐9 tumor regression on Day 9 following Pola administration. In vivo experiments (B–E) were conducted in DBA/2J mice. (F) Schematic diagram illustrating the relationship between the antitumor effect of Pola and innate immune cells.
    L1210 Mouse Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 582 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Innate Immune Cell Infiltration Induced by Polatuzumab Vedotin Contributes to the Antitumor Effect in Mouse Models"

    Article Title: Innate Immune Cell Infiltration Induced by Polatuzumab Vedotin Contributes to the Antitumor Effect in Mouse Models

    Journal: EJHaem

    doi: 10.1002/jha2.70219

    Pola‐induced infiltration of MΦs and NK cells contributes to the antitumor effect of Pola in the L1210‐hCD79b‐9 syngeneic mouse model. (A) Sensitivity of L1210 and L1210‐hCD79b‐9 cells to Pola at the indicated concentrations (3 replicates). The data represent the mean + SD. (B) Percentage of the area of CD68‐positive staining cells to the total area of tumor cells and (C) percentage of NCR1‐positive cells among tumor cells after 4 mg/kg ctrl IgG or 4 mg/kg Pola administration in the L1210‐hCD79b‐9 syngeneic mouse model ( n = 8). * p < 0.05 by Student's t ‐test. In dot plots, horizontal bars represent median values. (D) L1210‐hCD79b‐9 tumor growth curves from Day 0 to Day 9 after administration of 4 mg/kg ctrl IgG, 4 mg/kg Pola, or 4 mg/kg Pola plus clodronate liposomes plus anti‐asialo GM1 ( n = 6–7). (E) Numbers of mice presenting L1210‐hCD79b‐9 tumor regression on Day 9 following Pola administration. In vivo experiments (B–E) were conducted in DBA/2J mice. (F) Schematic diagram illustrating the relationship between the antitumor effect of Pola and innate immune cells.
    Figure Legend Snippet: Pola‐induced infiltration of MΦs and NK cells contributes to the antitumor effect of Pola in the L1210‐hCD79b‐9 syngeneic mouse model. (A) Sensitivity of L1210 and L1210‐hCD79b‐9 cells to Pola at the indicated concentrations (3 replicates). The data represent the mean + SD. (B) Percentage of the area of CD68‐positive staining cells to the total area of tumor cells and (C) percentage of NCR1‐positive cells among tumor cells after 4 mg/kg ctrl IgG or 4 mg/kg Pola administration in the L1210‐hCD79b‐9 syngeneic mouse model ( n = 8). * p < 0.05 by Student's t ‐test. In dot plots, horizontal bars represent median values. (D) L1210‐hCD79b‐9 tumor growth curves from Day 0 to Day 9 after administration of 4 mg/kg ctrl IgG, 4 mg/kg Pola, or 4 mg/kg Pola plus clodronate liposomes plus anti‐asialo GM1 ( n = 6–7). (E) Numbers of mice presenting L1210‐hCD79b‐9 tumor regression on Day 9 following Pola administration. In vivo experiments (B–E) were conducted in DBA/2J mice. (F) Schematic diagram illustrating the relationship between the antitumor effect of Pola and innate immune cells.

    Techniques Used: Staining, Liposomes, In Vivo



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    Pola‐induced infiltration of MΦs and NK cells contributes to the antitumor effect of Pola in the <t>L1210‐hCD79b‐9</t> syngeneic mouse model. (A) Sensitivity of L1210 and L1210‐hCD79b‐9 cells to Pola at the indicated concentrations (3 replicates). The data represent the mean + SD. (B) Percentage of the area of CD68‐positive staining cells to the total area of tumor cells and (C) percentage of NCR1‐positive cells among tumor cells after 4 mg/kg ctrl IgG or 4 mg/kg Pola administration in the L1210‐hCD79b‐9 syngeneic mouse model ( n = 8). * p < 0.05 by Student's t ‐test. In dot plots, horizontal bars represent median values. (D) L1210‐hCD79b‐9 tumor growth curves from Day 0 to Day 9 after administration of 4 mg/kg ctrl IgG, 4 mg/kg Pola, or 4 mg/kg Pola plus clodronate liposomes plus anti‐asialo GM1 ( n = 6–7). (E) Numbers of mice presenting L1210‐hCD79b‐9 tumor regression on Day 9 following Pola administration. In vivo experiments (B–E) were conducted in DBA/2J mice. (F) Schematic diagram illustrating the relationship between the antitumor effect of Pola and innate immune cells.
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    Pola‐induced infiltration of MΦs and NK cells contributes to the antitumor effect of Pola in the <t>L1210‐hCD79b‐9</t> syngeneic mouse model. (A) Sensitivity of L1210 and L1210‐hCD79b‐9 cells to Pola at the indicated concentrations (3 replicates). The data represent the mean + SD. (B) Percentage of the area of CD68‐positive staining cells to the total area of tumor cells and (C) percentage of NCR1‐positive cells among tumor cells after 4 mg/kg ctrl IgG or 4 mg/kg Pola administration in the L1210‐hCD79b‐9 syngeneic mouse model ( n = 8). * p < 0.05 by Student's t ‐test. In dot plots, horizontal bars represent median values. (D) L1210‐hCD79b‐9 tumor growth curves from Day 0 to Day 9 after administration of 4 mg/kg ctrl IgG, 4 mg/kg Pola, or 4 mg/kg Pola plus clodronate liposomes plus anti‐asialo GM1 ( n = 6–7). (E) Numbers of mice presenting L1210‐hCD79b‐9 tumor regression on Day 9 following Pola administration. In vivo experiments (B–E) were conducted in DBA/2J mice. (F) Schematic diagram illustrating the relationship between the antitumor effect of Pola and innate immune cells.
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    a, BiTNHER with a 3:1 SLAMF7:HER conjugation ratio had the maximum pro-phagocytosis effect of human THP-1 against HER2-expressing SK-BR-3 cancer cells in the presence of aCD47 (n=3). b, BiTNHER converted HER2/neu-expressing human (SK-BR-3) and mouse (EO771/E2) breast cancer cells into SLAMF7high cells and promoted human THP-1 or mouse (C57BL6 bone marrow) macrophage phagocytosis in the presence of aCD47, comparable with the SLAMF7-expressing mouse leukemia <t>L1210</t> cells (n=3). c, Anti-SLAMF7 antibody abrogated the pro-phagocytosis effect of BiTNHER and aCD47 on HER2-expressing cancer cells (n=3). d, Phagocytosis of CFSE-labelled HER2low EO771 and HER2high EO771/E2 mouse breast cancer cells and SLAMF7high L1210 <t>mouse</t> <t>leukemia</t> <t>cells</t> by mouse bone marrow macrophages in the presence of aCD47 after treatment with NP alone, NP with unconjugated anti-HER2 antibody and SLAMF7, or BiTNHER. Red, macrophages; green, cancer cells (scale bar, 50 μm). e, BiTNHER with aCD47 promotes macrophage phagocytosis against HER2-expressing breast cancer cells. f, Macrophages had increased antigen presentation of the H2kb-SIINFEKL complex after phagocytosis of BiTNHER -treated HER2-expressing EO771/E2-cOVA cells. Green, macrophages; red, H2kb-SIINFEKL complex (scale bar, 50 μm). g, Combination of BiTNHER and aCD47 increased macrophage antigen presentation of HER2-expressing cancer cells (n=4). h,i, BiTNHER with aCD47 promoted the priming of cOVA antigen-specific T cells (left) and induced a shift in naive T cells towards memory T cells (right) (n=4). For all figures, data are presented as mean±s.e.m.; **P<0.01, ***P<0.001, and ****P<0.0001 by one-way ANOVA with a Bonferroni post hoc correction. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 by unpaired Student’s t-test for the indicated comparisons; n.s., not significant.
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    Image Search Results


    Pola‐induced infiltration of MΦs and NK cells contributes to the antitumor effect of Pola in the L1210‐hCD79b‐9 syngeneic mouse model. (A) Sensitivity of L1210 and L1210‐hCD79b‐9 cells to Pola at the indicated concentrations (3 replicates). The data represent the mean + SD. (B) Percentage of the area of CD68‐positive staining cells to the total area of tumor cells and (C) percentage of NCR1‐positive cells among tumor cells after 4 mg/kg ctrl IgG or 4 mg/kg Pola administration in the L1210‐hCD79b‐9 syngeneic mouse model ( n = 8). * p < 0.05 by Student's t ‐test. In dot plots, horizontal bars represent median values. (D) L1210‐hCD79b‐9 tumor growth curves from Day 0 to Day 9 after administration of 4 mg/kg ctrl IgG, 4 mg/kg Pola, or 4 mg/kg Pola plus clodronate liposomes plus anti‐asialo GM1 ( n = 6–7). (E) Numbers of mice presenting L1210‐hCD79b‐9 tumor regression on Day 9 following Pola administration. In vivo experiments (B–E) were conducted in DBA/2J mice. (F) Schematic diagram illustrating the relationship between the antitumor effect of Pola and innate immune cells.

    Journal: EJHaem

    Article Title: Innate Immune Cell Infiltration Induced by Polatuzumab Vedotin Contributes to the Antitumor Effect in Mouse Models

    doi: 10.1002/jha2.70219

    Figure Lengend Snippet: Pola‐induced infiltration of MΦs and NK cells contributes to the antitumor effect of Pola in the L1210‐hCD79b‐9 syngeneic mouse model. (A) Sensitivity of L1210 and L1210‐hCD79b‐9 cells to Pola at the indicated concentrations (3 replicates). The data represent the mean + SD. (B) Percentage of the area of CD68‐positive staining cells to the total area of tumor cells and (C) percentage of NCR1‐positive cells among tumor cells after 4 mg/kg ctrl IgG or 4 mg/kg Pola administration in the L1210‐hCD79b‐9 syngeneic mouse model ( n = 8). * p < 0.05 by Student's t ‐test. In dot plots, horizontal bars represent median values. (D) L1210‐hCD79b‐9 tumor growth curves from Day 0 to Day 9 after administration of 4 mg/kg ctrl IgG, 4 mg/kg Pola, or 4 mg/kg Pola plus clodronate liposomes plus anti‐asialo GM1 ( n = 6–7). (E) Numbers of mice presenting L1210‐hCD79b‐9 tumor regression on Day 9 following Pola administration. In vivo experiments (B–E) were conducted in DBA/2J mice. (F) Schematic diagram illustrating the relationship between the antitumor effect of Pola and innate immune cells.

    Article Snippet: The DB (human) and L1210 (mouse) cell lines were purchased from the American Type Culture Collection.

    Techniques: Staining, Liposomes, In Vivo

    a, BiTNHER with a 3:1 SLAMF7:HER conjugation ratio had the maximum pro-phagocytosis effect of human THP-1 against HER2-expressing SK-BR-3 cancer cells in the presence of aCD47 (n=3). b, BiTNHER converted HER2/neu-expressing human (SK-BR-3) and mouse (EO771/E2) breast cancer cells into SLAMF7high cells and promoted human THP-1 or mouse (C57BL6 bone marrow) macrophage phagocytosis in the presence of aCD47, comparable with the SLAMF7-expressing mouse leukemia L1210 cells (n=3). c, Anti-SLAMF7 antibody abrogated the pro-phagocytosis effect of BiTNHER and aCD47 on HER2-expressing cancer cells (n=3). d, Phagocytosis of CFSE-labelled HER2low EO771 and HER2high EO771/E2 mouse breast cancer cells and SLAMF7high L1210 mouse leukemia cells by mouse bone marrow macrophages in the presence of aCD47 after treatment with NP alone, NP with unconjugated anti-HER2 antibody and SLAMF7, or BiTNHER. Red, macrophages; green, cancer cells (scale bar, 50 μm). e, BiTNHER with aCD47 promotes macrophage phagocytosis against HER2-expressing breast cancer cells. f, Macrophages had increased antigen presentation of the H2kb-SIINFEKL complex after phagocytosis of BiTNHER -treated HER2-expressing EO771/E2-cOVA cells. Green, macrophages; red, H2kb-SIINFEKL complex (scale bar, 50 μm). g, Combination of BiTNHER and aCD47 increased macrophage antigen presentation of HER2-expressing cancer cells (n=4). h,i, BiTNHER with aCD47 promoted the priming of cOVA antigen-specific T cells (left) and induced a shift in naive T cells towards memory T cells (right) (n=4). For all figures, data are presented as mean±s.e.m.; **P<0.01, ***P<0.001, and ****P<0.0001 by one-way ANOVA with a Bonferroni post hoc correction. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 by unpaired Student’s t-test for the indicated comparisons; n.s., not significant.

    Journal: Nature nanotechnology

    Article Title: Immunological conversion of solid tumours using a bispecific nanobioconjugate for cancer immunotherapy

    doi: 10.1038/s41565-022-01245-7

    Figure Lengend Snippet: a, BiTNHER with a 3:1 SLAMF7:HER conjugation ratio had the maximum pro-phagocytosis effect of human THP-1 against HER2-expressing SK-BR-3 cancer cells in the presence of aCD47 (n=3). b, BiTNHER converted HER2/neu-expressing human (SK-BR-3) and mouse (EO771/E2) breast cancer cells into SLAMF7high cells and promoted human THP-1 or mouse (C57BL6 bone marrow) macrophage phagocytosis in the presence of aCD47, comparable with the SLAMF7-expressing mouse leukemia L1210 cells (n=3). c, Anti-SLAMF7 antibody abrogated the pro-phagocytosis effect of BiTNHER and aCD47 on HER2-expressing cancer cells (n=3). d, Phagocytosis of CFSE-labelled HER2low EO771 and HER2high EO771/E2 mouse breast cancer cells and SLAMF7high L1210 mouse leukemia cells by mouse bone marrow macrophages in the presence of aCD47 after treatment with NP alone, NP with unconjugated anti-HER2 antibody and SLAMF7, or BiTNHER. Red, macrophages; green, cancer cells (scale bar, 50 μm). e, BiTNHER with aCD47 promotes macrophage phagocytosis against HER2-expressing breast cancer cells. f, Macrophages had increased antigen presentation of the H2kb-SIINFEKL complex after phagocytosis of BiTNHER -treated HER2-expressing EO771/E2-cOVA cells. Green, macrophages; red, H2kb-SIINFEKL complex (scale bar, 50 μm). g, Combination of BiTNHER and aCD47 increased macrophage antigen presentation of HER2-expressing cancer cells (n=4). h,i, BiTNHER with aCD47 promoted the priming of cOVA antigen-specific T cells (left) and induced a shift in naive T cells towards memory T cells (right) (n=4). For all figures, data are presented as mean±s.e.m.; **P<0.01, ***P<0.001, and ****P<0.0001 by one-way ANOVA with a Bonferroni post hoc correction. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 by unpaired Student’s t-test for the indicated comparisons; n.s., not significant.

    Article Snippet: The human mammary carcinoma cell lines SK-BR-3 (HTB-30) and MDA-MD-468 (HTB-132), the human monocyte cell line THP-1 (TIB-202), the mouse mammary carcinoma cell lines 4T1 (CRL-2539) and EO771 (CRL-3461), and the mouse B-cell lymphocytic leukaemia cell line L1210 (CCL-219) were obtained from the American Type Culture Collection.

    Techniques: Conjugation Assay, Expressing, Immunopeptidomics