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nk92 cd16 nk cells  (ATCC)


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    ATCC nk92 cd16 nk cells
    ( A – C ) Cell viability (MTT) assays of ( A ) SKOV3, ( B ) SNU-119, and ( C ) SNU-251 cell lines treated with various samfenet concentrations for 72 h. Three independently repeated experiments were performed with similar results. ( D – E ) The NK cytotoxicity assay in the presence or absence of samfenet was analyzed using CFSE-7AAD assay. Target cells [( D ) SKOV3, ( E ) SNU-119, and ( F ) SNU-251] and effector cells <t>(NK92-CD16</t> cells) were co-cultured at 1:1, 5:1, and 10:1 E/T ratios for 4 h with 5 mg/mL of samfenet. Three independently repeated experiments were performed with similar results. Error bars represent the standard deviations of three independent experiments. Student’s t -test between NK92-CD16 and Samfenet+NK92-CD16: * p < 0.05, ** p < 0.01. Abbreviation: ns, not significant. ( G ) Colony formation assay in the presence or absence of samfenet and NK92-CD16 with or without CD16 blocking. Target cells (SKOV3, SNU-119, SNU-251) and effector cells (NK92-CD16 cells) were co-cultured at 10:1 E/T ratio for 4 h with 400 ug/mL of samfenet. The photographs were taken 10 days after culture. Abbreviation: Samf: Samfenet; NK: NK92-CD16; aCD16: CD16 antibody.
    Nk92 Cd16 Nk Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Trastuzumab-Mediated Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC) Enhances Natural Killer Cell Cytotoxicity in HER2-Overexpressing Ovarian Cancer"

    Article Title: Trastuzumab-Mediated Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC) Enhances Natural Killer Cell Cytotoxicity in HER2-Overexpressing Ovarian Cancer

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms252111733

    ( A – C ) Cell viability (MTT) assays of ( A ) SKOV3, ( B ) SNU-119, and ( C ) SNU-251 cell lines treated with various samfenet concentrations for 72 h. Three independently repeated experiments were performed with similar results. ( D – E ) The NK cytotoxicity assay in the presence or absence of samfenet was analyzed using CFSE-7AAD assay. Target cells [( D ) SKOV3, ( E ) SNU-119, and ( F ) SNU-251] and effector cells (NK92-CD16 cells) were co-cultured at 1:1, 5:1, and 10:1 E/T ratios for 4 h with 5 mg/mL of samfenet. Three independently repeated experiments were performed with similar results. Error bars represent the standard deviations of three independent experiments. Student’s t -test between NK92-CD16 and Samfenet+NK92-CD16: * p < 0.05, ** p < 0.01. Abbreviation: ns, not significant. ( G ) Colony formation assay in the presence or absence of samfenet and NK92-CD16 with or without CD16 blocking. Target cells (SKOV3, SNU-119, SNU-251) and effector cells (NK92-CD16 cells) were co-cultured at 10:1 E/T ratio for 4 h with 400 ug/mL of samfenet. The photographs were taken 10 days after culture. Abbreviation: Samf: Samfenet; NK: NK92-CD16; aCD16: CD16 antibody.
    Figure Legend Snippet: ( A – C ) Cell viability (MTT) assays of ( A ) SKOV3, ( B ) SNU-119, and ( C ) SNU-251 cell lines treated with various samfenet concentrations for 72 h. Three independently repeated experiments were performed with similar results. ( D – E ) The NK cytotoxicity assay in the presence or absence of samfenet was analyzed using CFSE-7AAD assay. Target cells [( D ) SKOV3, ( E ) SNU-119, and ( F ) SNU-251] and effector cells (NK92-CD16 cells) were co-cultured at 1:1, 5:1, and 10:1 E/T ratios for 4 h with 5 mg/mL of samfenet. Three independently repeated experiments were performed with similar results. Error bars represent the standard deviations of three independent experiments. Student’s t -test between NK92-CD16 and Samfenet+NK92-CD16: * p < 0.05, ** p < 0.01. Abbreviation: ns, not significant. ( G ) Colony formation assay in the presence or absence of samfenet and NK92-CD16 with or without CD16 blocking. Target cells (SKOV3, SNU-119, SNU-251) and effector cells (NK92-CD16 cells) were co-cultured at 10:1 E/T ratio for 4 h with 400 ug/mL of samfenet. The photographs were taken 10 days after culture. Abbreviation: Samf: Samfenet; NK: NK92-CD16; aCD16: CD16 antibody.

    Techniques Used: Cytotoxicity Assay, Cell Culture, Colony Assay, Blocking Assay

    ( A ) Treatment schedule for main in vivo efficacy testing using HER2-overexpressing PDTX model (PDTX 18-4). ( B ) The average relative tumor growth of HER2-overexpressing PDTX 18-4 tumors, which were treated with indicated drugs, in the preliminary in vivo test using primary NK cells. Error bars represent the standard error of the mean (SEM) of two tumors per group. ( C ) The average tumor volume of HER2-overexpressing PDTX 18-4 tumors, which were treated with indicated drugs, in the main in vivo test using NK92-CD16 cells. Error bars represent the SEM of five tumors per group. Student’s t -test: * p < 0.05. Abbreviation: ns, not significant. ( D ) Tumor growth curves of individual mice in the indicated treatment groups of the HER2-overexpressing PDTX 18-4 model. ( E ) Average body weight of mice with indicated groups. Error bars represent the standard deviations of five mice per group. ( F ) Gross harvested tumor. ( G ) TUNEL assay using PDTX 18-4 xenografted tumor after sacrifice. Staining images per group are shown, and bar graphs represent the average number of apoptotic cells per group in five random, non-overlapping fields at 400× magnification. Data are presented as mean ± SD. Student’s t -test: *** p < 0.001. Abbreviation: Con: control; Samf: samfenet; NK: NK92-CD16; Combi: combination. ( H ) Immunohistochemistry for human leukocyte common antigen (LCA) using PDTX 18-4 xenografted tumor after sacrifice. Staining images per group are shown, and bar graph represents the average number of LCA-positive cells per group in five random, non-overlapping fields at 400× magnification. Data are presented as mean ± SD. Student’s t -test: ** p < 0.01. Abbreviation: Con: control; Samf: samfenet; NK: NK92-CD16; Combi: combination.
    Figure Legend Snippet: ( A ) Treatment schedule for main in vivo efficacy testing using HER2-overexpressing PDTX model (PDTX 18-4). ( B ) The average relative tumor growth of HER2-overexpressing PDTX 18-4 tumors, which were treated with indicated drugs, in the preliminary in vivo test using primary NK cells. Error bars represent the standard error of the mean (SEM) of two tumors per group. ( C ) The average tumor volume of HER2-overexpressing PDTX 18-4 tumors, which were treated with indicated drugs, in the main in vivo test using NK92-CD16 cells. Error bars represent the SEM of five tumors per group. Student’s t -test: * p < 0.05. Abbreviation: ns, not significant. ( D ) Tumor growth curves of individual mice in the indicated treatment groups of the HER2-overexpressing PDTX 18-4 model. ( E ) Average body weight of mice with indicated groups. Error bars represent the standard deviations of five mice per group. ( F ) Gross harvested tumor. ( G ) TUNEL assay using PDTX 18-4 xenografted tumor after sacrifice. Staining images per group are shown, and bar graphs represent the average number of apoptotic cells per group in five random, non-overlapping fields at 400× magnification. Data are presented as mean ± SD. Student’s t -test: *** p < 0.001. Abbreviation: Con: control; Samf: samfenet; NK: NK92-CD16; Combi: combination. ( H ) Immunohistochemistry for human leukocyte common antigen (LCA) using PDTX 18-4 xenografted tumor after sacrifice. Staining images per group are shown, and bar graph represents the average number of LCA-positive cells per group in five random, non-overlapping fields at 400× magnification. Data are presented as mean ± SD. Student’s t -test: ** p < 0.01. Abbreviation: Con: control; Samf: samfenet; NK: NK92-CD16; Combi: combination.

    Techniques Used: In Vivo, TUNEL Assay, Staining, Control, Immunohistochemistry



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    a CD16a IHC of representative high-risk ( MYCN amplified; left ) and low-risk ( right ) neuroblastoma tumors, respectively. Scales bars are indicated. b CD3 IHC of the same tumors shown in ( a ). Scales bars are indicated. c Percentage of CD16a + cells in tumors stratified by International Neuroblastoma Risk Group (INRG) (low/intermediate; n = 22 vs. high; n = 23), previous chemotherapy treatment [diagnosis; n = 25 vs. post-chemo (only high-risk); n = 10] and MYCN amplification (non-amplified; n = 14 vs. amplified; n = 8) included in the TMA. * P = 0.038 and ** P = 0.004 (Unpaired t -test; two-tailed). Means and SDs are shown. d Percentage of CD3 + cells in tumors stratified by INRG (low/intermediate; n = 22 vs. high; n = 24), previous chemotherapy treatment [diagnosis; n = 26 vs. post-chemo (only high-risk); n = 9] and MYCN amplification (non-amplified; n = 15 vs. amplified; n = 9) included in the TMA. * P = 0.034 and ** P = 0.027 (Unpaired t -test; two-tailed). MS neuroblastomas were excluded from the analyses in ( c and d ). Means and SDs are shown. e Expression of PTPRC (encoding CD45), <t>FCGR3A</t> (encoding CD16a), CD68 (defining macrophages) and NKG7 (defining NK-cells) in 2 neuroblastoma single cell datasets (6442 and 13,281 cells, respectively). SingleR analysis was also used to label different cell types [NK-cells and T-cells (helper and cytotoxic); right ]. f Heatmap showing single-cell expression profiles ( n = 16 NK-related genes) in the subset of NK-cells identified in dataset in ( e ) (top). Red box indicates the subpopulation of NK-cells with potential dysfunctional properties. FCGR3A is highlighted in bold. g Percentage of CD16a-positive cells in immune cell subsets present in neuroblastoma-infiltrated bone marrows. P values are shown in graph (One-way ANOVA plus Dunn’s multiple comparison test). Means and SDs are shown ( n = 9). h Immune cell types present in neuroblastoma-infiltrated bone marrows. Percentage of total CD45 cells is indicated. P values are shown in graph (One-way ANOVA plus Dunn’s multiple comparison test). Means and SDs are shown ( n = 9). Gating strategies are shown in Supplementary Fig. . i ( left ) Dot plots showing co-expression of CD56 and CD16a on NK-cells isolated from a neuroblastoma-infiltrating patient BM specimen. ( right ) Flow cytometry histograms showing TIGIT and LAG3 levels on BM-derived NK-cells. For further clinical information see Supplementary Table . US unstained, inter intermediate, chemo chemotherapy. Source data are provided as a Source Data file.
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    nk  (ATCC)
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    a CD16a IHC of representative high-risk ( MYCN amplified; left ) and low-risk ( right ) neuroblastoma tumors, respectively. Scales bars are indicated. b CD3 IHC of the same tumors shown in ( a ). Scales bars are indicated. c Percentage of CD16a + cells in tumors stratified by International Neuroblastoma Risk Group (INRG) (low/intermediate; n = 22 vs. high; n = 23), previous chemotherapy treatment [diagnosis; n = 25 vs. post-chemo (only high-risk); n = 10] and MYCN amplification (non-amplified; n = 14 vs. amplified; n = 8) included in the TMA. * P = 0.038 and ** P = 0.004 (Unpaired t -test; two-tailed). Means and SDs are shown. d Percentage of CD3 + cells in tumors stratified by INRG (low/intermediate; n = 22 vs. high; n = 24), previous chemotherapy treatment [diagnosis; n = 26 vs. post-chemo (only high-risk); n = 9] and MYCN amplification (non-amplified; n = 15 vs. amplified; n = 9) included in the TMA. * P = 0.034 and ** P = 0.027 (Unpaired t -test; two-tailed). MS neuroblastomas were excluded from the analyses in ( c and d ). Means and SDs are shown. e Expression of PTPRC (encoding CD45), <t>FCGR3A</t> (encoding CD16a), CD68 (defining macrophages) and NKG7 (defining NK-cells) in 2 neuroblastoma single cell datasets (6442 and 13,281 cells, respectively). SingleR analysis was also used to label different cell types [NK-cells and T-cells (helper and cytotoxic); right ]. f Heatmap showing single-cell expression profiles ( n = 16 NK-related genes) in the subset of NK-cells identified in dataset in ( e ) (top). Red box indicates the subpopulation of NK-cells with potential dysfunctional properties. FCGR3A is highlighted in bold. g Percentage of CD16a-positive cells in immune cell subsets present in neuroblastoma-infiltrated bone marrows. P values are shown in graph (One-way ANOVA plus Dunn’s multiple comparison test). Means and SDs are shown ( n = 9). h Immune cell types present in neuroblastoma-infiltrated bone marrows. Percentage of total CD45 cells is indicated. P values are shown in graph (One-way ANOVA plus Dunn’s multiple comparison test). Means and SDs are shown ( n = 9). Gating strategies are shown in Supplementary Fig. . i ( left ) Dot plots showing co-expression of CD56 and CD16a on NK-cells isolated from a neuroblastoma-infiltrating patient BM specimen. ( right ) Flow cytometry histograms showing TIGIT and LAG3 levels on BM-derived NK-cells. For further clinical information see Supplementary Table . US unstained, inter intermediate, chemo chemotherapy. Source data are provided as a Source Data file.
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    ( A – C ) Cell viability (MTT) assays of ( A ) SKOV3, ( B ) SNU-119, and ( C ) SNU-251 cell lines treated with various samfenet concentrations for 72 h. Three independently repeated experiments were performed with similar results. ( D – E ) The NK cytotoxicity assay in the presence or absence of samfenet was analyzed using CFSE-7AAD assay. Target cells [( D ) SKOV3, ( E ) SNU-119, and ( F ) SNU-251] and effector cells (NK92-CD16 cells) were co-cultured at 1:1, 5:1, and 10:1 E/T ratios for 4 h with 5 mg/mL of samfenet. Three independently repeated experiments were performed with similar results. Error bars represent the standard deviations of three independent experiments. Student’s t -test between NK92-CD16 and Samfenet+NK92-CD16: * p < 0.05, ** p < 0.01. Abbreviation: ns, not significant. ( G ) Colony formation assay in the presence or absence of samfenet and NK92-CD16 with or without CD16 blocking. Target cells (SKOV3, SNU-119, SNU-251) and effector cells (NK92-CD16 cells) were co-cultured at 10:1 E/T ratio for 4 h with 400 ug/mL of samfenet. The photographs were taken 10 days after culture. Abbreviation: Samf: Samfenet; NK: NK92-CD16; aCD16: CD16 antibody.

    Journal: International Journal of Molecular Sciences

    Article Title: Trastuzumab-Mediated Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC) Enhances Natural Killer Cell Cytotoxicity in HER2-Overexpressing Ovarian Cancer

    doi: 10.3390/ijms252111733

    Figure Lengend Snippet: ( A – C ) Cell viability (MTT) assays of ( A ) SKOV3, ( B ) SNU-119, and ( C ) SNU-251 cell lines treated with various samfenet concentrations for 72 h. Three independently repeated experiments were performed with similar results. ( D – E ) The NK cytotoxicity assay in the presence or absence of samfenet was analyzed using CFSE-7AAD assay. Target cells [( D ) SKOV3, ( E ) SNU-119, and ( F ) SNU-251] and effector cells (NK92-CD16 cells) were co-cultured at 1:1, 5:1, and 10:1 E/T ratios for 4 h with 5 mg/mL of samfenet. Three independently repeated experiments were performed with similar results. Error bars represent the standard deviations of three independent experiments. Student’s t -test between NK92-CD16 and Samfenet+NK92-CD16: * p < 0.05, ** p < 0.01. Abbreviation: ns, not significant. ( G ) Colony formation assay in the presence or absence of samfenet and NK92-CD16 with or without CD16 blocking. Target cells (SKOV3, SNU-119, SNU-251) and effector cells (NK92-CD16 cells) were co-cultured at 10:1 E/T ratio for 4 h with 400 ug/mL of samfenet. The photographs were taken 10 days after culture. Abbreviation: Samf: Samfenet; NK: NK92-CD16; aCD16: CD16 antibody.

    Article Snippet: CD16-expressing (NK92-CD16) NK cells were kindly supplied by Semi Kim from Korea University, who purchased cells from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Cytotoxicity Assay, Cell Culture, Colony Assay, Blocking Assay

    ( A ) Treatment schedule for main in vivo efficacy testing using HER2-overexpressing PDTX model (PDTX 18-4). ( B ) The average relative tumor growth of HER2-overexpressing PDTX 18-4 tumors, which were treated with indicated drugs, in the preliminary in vivo test using primary NK cells. Error bars represent the standard error of the mean (SEM) of two tumors per group. ( C ) The average tumor volume of HER2-overexpressing PDTX 18-4 tumors, which were treated with indicated drugs, in the main in vivo test using NK92-CD16 cells. Error bars represent the SEM of five tumors per group. Student’s t -test: * p < 0.05. Abbreviation: ns, not significant. ( D ) Tumor growth curves of individual mice in the indicated treatment groups of the HER2-overexpressing PDTX 18-4 model. ( E ) Average body weight of mice with indicated groups. Error bars represent the standard deviations of five mice per group. ( F ) Gross harvested tumor. ( G ) TUNEL assay using PDTX 18-4 xenografted tumor after sacrifice. Staining images per group are shown, and bar graphs represent the average number of apoptotic cells per group in five random, non-overlapping fields at 400× magnification. Data are presented as mean ± SD. Student’s t -test: *** p < 0.001. Abbreviation: Con: control; Samf: samfenet; NK: NK92-CD16; Combi: combination. ( H ) Immunohistochemistry for human leukocyte common antigen (LCA) using PDTX 18-4 xenografted tumor after sacrifice. Staining images per group are shown, and bar graph represents the average number of LCA-positive cells per group in five random, non-overlapping fields at 400× magnification. Data are presented as mean ± SD. Student’s t -test: ** p < 0.01. Abbreviation: Con: control; Samf: samfenet; NK: NK92-CD16; Combi: combination.

    Journal: International Journal of Molecular Sciences

    Article Title: Trastuzumab-Mediated Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC) Enhances Natural Killer Cell Cytotoxicity in HER2-Overexpressing Ovarian Cancer

    doi: 10.3390/ijms252111733

    Figure Lengend Snippet: ( A ) Treatment schedule for main in vivo efficacy testing using HER2-overexpressing PDTX model (PDTX 18-4). ( B ) The average relative tumor growth of HER2-overexpressing PDTX 18-4 tumors, which were treated with indicated drugs, in the preliminary in vivo test using primary NK cells. Error bars represent the standard error of the mean (SEM) of two tumors per group. ( C ) The average tumor volume of HER2-overexpressing PDTX 18-4 tumors, which were treated with indicated drugs, in the main in vivo test using NK92-CD16 cells. Error bars represent the SEM of five tumors per group. Student’s t -test: * p < 0.05. Abbreviation: ns, not significant. ( D ) Tumor growth curves of individual mice in the indicated treatment groups of the HER2-overexpressing PDTX 18-4 model. ( E ) Average body weight of mice with indicated groups. Error bars represent the standard deviations of five mice per group. ( F ) Gross harvested tumor. ( G ) TUNEL assay using PDTX 18-4 xenografted tumor after sacrifice. Staining images per group are shown, and bar graphs represent the average number of apoptotic cells per group in five random, non-overlapping fields at 400× magnification. Data are presented as mean ± SD. Student’s t -test: *** p < 0.001. Abbreviation: Con: control; Samf: samfenet; NK: NK92-CD16; Combi: combination. ( H ) Immunohistochemistry for human leukocyte common antigen (LCA) using PDTX 18-4 xenografted tumor after sacrifice. Staining images per group are shown, and bar graph represents the average number of LCA-positive cells per group in five random, non-overlapping fields at 400× magnification. Data are presented as mean ± SD. Student’s t -test: ** p < 0.01. Abbreviation: Con: control; Samf: samfenet; NK: NK92-CD16; Combi: combination.

    Article Snippet: CD16-expressing (NK92-CD16) NK cells were kindly supplied by Semi Kim from Korea University, who purchased cells from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: In Vivo, TUNEL Assay, Staining, Control, Immunohistochemistry

    Tz‐pHLIP‐mediated TCO‐IgG recruitment activates effector cells via FCγRIIIa. DLD‐1 cells were treated at pH 7.4 or 6.0 with 5 μM Tz‐pHLIP and sequentially with 25 μg/mL TCO‐IgG. Levels of CD16a activation were measured as a bioluminescent signal corresponding to luciferase activity following 6 hours of incubation with Jurkat‐CD16 cells at a 2 : 1 effector‐to‐target ratio. CD16a activation is represented as the % increase in luminescence intensity with respect to the untreated control at pH 7.4. (DLD‐1 cells treated without peptide or TCO‐IgG and incubated with Jurkat‐CD16 cells at a 2 : 1 E : T). Data are shown as mean±SD (n=6). The level of significance (two‐way ANOVA with Tukey's multiple comparisons correction, alpha=0.05) is shown.

    Journal: Chemmedchem

    Article Title: Selective Recruitment of Antibodies to Cancer Cells and Immune Cell‐mediated Killing via In Situ Click Chemistry

    doi: 10.1002/cmdc.202400356

    Figure Lengend Snippet: Tz‐pHLIP‐mediated TCO‐IgG recruitment activates effector cells via FCγRIIIa. DLD‐1 cells were treated at pH 7.4 or 6.0 with 5 μM Tz‐pHLIP and sequentially with 25 μg/mL TCO‐IgG. Levels of CD16a activation were measured as a bioluminescent signal corresponding to luciferase activity following 6 hours of incubation with Jurkat‐CD16 cells at a 2 : 1 effector‐to‐target ratio. CD16a activation is represented as the % increase in luminescence intensity with respect to the untreated control at pH 7.4. (DLD‐1 cells treated without peptide or TCO‐IgG and incubated with Jurkat‐CD16 cells at a 2 : 1 E : T). Data are shown as mean±SD (n=6). The level of significance (two‐way ANOVA with Tukey's multiple comparisons correction, alpha=0.05) is shown.

    Article Snippet: Engineered human F176 V CD16+ natural killer NK‐92 cells (haNK cells; ATCC PTA‐6967) were cultured in minimum essential medium (MEMα) without nucleosides supplemented with 0.1 mM 2‐mercaptoethanol, 0.2 mM inositol, 0.02 mM folic acid, 12.5 % FBS, 12.5 % horse serum, 100–200 units/mL interleukin‐2 (IL‐2), 100 units/mL penicillin, and 0.1 mg/mL streptomycin.

    Techniques: Activation Assay, Luciferase, Activity Assay, Incubation, Control

    a CD16a IHC of representative high-risk ( MYCN amplified; left ) and low-risk ( right ) neuroblastoma tumors, respectively. Scales bars are indicated. b CD3 IHC of the same tumors shown in ( a ). Scales bars are indicated. c Percentage of CD16a + cells in tumors stratified by International Neuroblastoma Risk Group (INRG) (low/intermediate; n = 22 vs. high; n = 23), previous chemotherapy treatment [diagnosis; n = 25 vs. post-chemo (only high-risk); n = 10] and MYCN amplification (non-amplified; n = 14 vs. amplified; n = 8) included in the TMA. * P = 0.038 and ** P = 0.004 (Unpaired t -test; two-tailed). Means and SDs are shown. d Percentage of CD3 + cells in tumors stratified by INRG (low/intermediate; n = 22 vs. high; n = 24), previous chemotherapy treatment [diagnosis; n = 26 vs. post-chemo (only high-risk); n = 9] and MYCN amplification (non-amplified; n = 15 vs. amplified; n = 9) included in the TMA. * P = 0.034 and ** P = 0.027 (Unpaired t -test; two-tailed). MS neuroblastomas were excluded from the analyses in ( c and d ). Means and SDs are shown. e Expression of PTPRC (encoding CD45), FCGR3A (encoding CD16a), CD68 (defining macrophages) and NKG7 (defining NK-cells) in 2 neuroblastoma single cell datasets (6442 and 13,281 cells, respectively). SingleR analysis was also used to label different cell types [NK-cells and T-cells (helper and cytotoxic); right ]. f Heatmap showing single-cell expression profiles ( n = 16 NK-related genes) in the subset of NK-cells identified in dataset in ( e ) (top). Red box indicates the subpopulation of NK-cells with potential dysfunctional properties. FCGR3A is highlighted in bold. g Percentage of CD16a-positive cells in immune cell subsets present in neuroblastoma-infiltrated bone marrows. P values are shown in graph (One-way ANOVA plus Dunn’s multiple comparison test). Means and SDs are shown ( n = 9). h Immune cell types present in neuroblastoma-infiltrated bone marrows. Percentage of total CD45 cells is indicated. P values are shown in graph (One-way ANOVA plus Dunn’s multiple comparison test). Means and SDs are shown ( n = 9). Gating strategies are shown in Supplementary Fig. . i ( left ) Dot plots showing co-expression of CD56 and CD16a on NK-cells isolated from a neuroblastoma-infiltrating patient BM specimen. ( right ) Flow cytometry histograms showing TIGIT and LAG3 levels on BM-derived NK-cells. For further clinical information see Supplementary Table . US unstained, inter intermediate, chemo chemotherapy. Source data are provided as a Source Data file.

    Journal: Nature Communications

    Article Title: CAR T-cell-mediated delivery of bispecific innate immune cell engagers for neuroblastoma

    doi: 10.1038/s41467-024-51337-2

    Figure Lengend Snippet: a CD16a IHC of representative high-risk ( MYCN amplified; left ) and low-risk ( right ) neuroblastoma tumors, respectively. Scales bars are indicated. b CD3 IHC of the same tumors shown in ( a ). Scales bars are indicated. c Percentage of CD16a + cells in tumors stratified by International Neuroblastoma Risk Group (INRG) (low/intermediate; n = 22 vs. high; n = 23), previous chemotherapy treatment [diagnosis; n = 25 vs. post-chemo (only high-risk); n = 10] and MYCN amplification (non-amplified; n = 14 vs. amplified; n = 8) included in the TMA. * P = 0.038 and ** P = 0.004 (Unpaired t -test; two-tailed). Means and SDs are shown. d Percentage of CD3 + cells in tumors stratified by INRG (low/intermediate; n = 22 vs. high; n = 24), previous chemotherapy treatment [diagnosis; n = 26 vs. post-chemo (only high-risk); n = 9] and MYCN amplification (non-amplified; n = 15 vs. amplified; n = 9) included in the TMA. * P = 0.034 and ** P = 0.027 (Unpaired t -test; two-tailed). MS neuroblastomas were excluded from the analyses in ( c and d ). Means and SDs are shown. e Expression of PTPRC (encoding CD45), FCGR3A (encoding CD16a), CD68 (defining macrophages) and NKG7 (defining NK-cells) in 2 neuroblastoma single cell datasets (6442 and 13,281 cells, respectively). SingleR analysis was also used to label different cell types [NK-cells and T-cells (helper and cytotoxic); right ]. f Heatmap showing single-cell expression profiles ( n = 16 NK-related genes) in the subset of NK-cells identified in dataset in ( e ) (top). Red box indicates the subpopulation of NK-cells with potential dysfunctional properties. FCGR3A is highlighted in bold. g Percentage of CD16a-positive cells in immune cell subsets present in neuroblastoma-infiltrated bone marrows. P values are shown in graph (One-way ANOVA plus Dunn’s multiple comparison test). Means and SDs are shown ( n = 9). h Immune cell types present in neuroblastoma-infiltrated bone marrows. Percentage of total CD45 cells is indicated. P values are shown in graph (One-way ANOVA plus Dunn’s multiple comparison test). Means and SDs are shown ( n = 9). Gating strategies are shown in Supplementary Fig. . i ( left ) Dot plots showing co-expression of CD56 and CD16a on NK-cells isolated from a neuroblastoma-infiltrating patient BM specimen. ( right ) Flow cytometry histograms showing TIGIT and LAG3 levels on BM-derived NK-cells. For further clinical information see Supplementary Table . US unstained, inter intermediate, chemo chemotherapy. Source data are provided as a Source Data file.

    Article Snippet: HEK293T and NK92-GFP-CD16 176V cell lines were obtained from ATCC (Catalog No. CRL-3216 and PTA-8836, respectively).

    Techniques: Amplification, Two Tailed Test, Expressing, Comparison, Isolation, Flow Cytometry, Derivative Assay

    a Graphical illustration of T-cell GPC2.CAR expression and GD2.BiCE secretion. b Schematic representation of transgenes for two BiCE-secreting GPC2.CAR constructs targeting GD2 and CD19 (GPC2.CAR-GD2.BiCE and GPC2.CAR-CD19.BiCE, respectively), as well as single GPC2.CAR, CD19.CAR and GD2.BiCE constructs. c Detection of GD2 BiCE by western blot (His-tag) in cSN from HEK293T cells transfected with GPC2.CAR-GD2.BiCE vector. d Binding assays detecting secondary His-tag expression on tumor cells incubated with cSN from HEK293T cells transfected with different constructs as indicated. e Correlation between GD2 BiCE binding and GD2 cell surface expression in NB cell lines. Spearman correlation (two-tailed). f Illustration ( left ) and histograms ( right ) of binding assay evaluating human recombinant CD16a protein binding to tumor cells incubated with different CAR construct cSNs. g Illustration ( left ) and histograms ( right ) of binding assay evaluating 1A7 binding to human primary NK-cells or T-cells incubated with different CAR construct cSNs. 1, control medium; 2, GPC2.CAR; 3, GPC2.CAR-CD19.BiCE; and 4, GPC2.CAR-GD2.BiCE in ( d , f , and g ). h NK-cell-mediated specific lysis of NB-EbC1 cells in the presence of cSNs (5 ng/mL of His-tagged BiCE), or dinutuximab (10 µg/mL) as a positive control. * P = 0.0009 and ** P = 0.0028 (One-way ANOVA plus Tukey’s multiple comparison test). Means and SDs are shown ( n = 3 independent donors). i Co-expression of CD107a and CD69 by flow cytometry in NK-cells from the cytotoxicity experiment in ( h ). * P = 0.0003 (One-way ANOVA plus Tukey’s multiple comparison test). Means and SDs are shown ( n = 3 independent donors). j IFN-γ levels measured by ELISA in NK-cell supernatants from the cytotoxicity experiment in ( h ). * P = 0.0028 (One-way ANOVA plus Tukey’s multiple comparison test). Means and SDs are shown ( n = 3 independent donors). k Polyfunctionality pie charts indicating the percentage of single NK-cells secreting 1 or more cytokine when cultured alone or in the presence of NB-EbC1 cells together with GD2 BiCE, CD19 BiCE or dinutuximab as in ( h ). l NK92 WT vs. NK92-CD16a cell cytotoxicity against NB-EbC1 cells co-incubated with different cSNs or dinutuximab (10 µg/mL) as a positive control after 24 hours at a 10:1 E:T ratio. Means and SDs are shown (n = 3 technical replicates). m ( left ) Percentage of CD107a + NK-cells isolated from either neuroblastoma-infiltrating BM aspirates or peripheral blood of healthy donors after 24 hours of co-incubation with NB-EbC1 cells and cSNs (from GPC2.CAR-GD2.BiCE or GPC2.CAR-CD19.BiCE; 5 ng/mL). * P = 0.0139 and ** P < 0.0001 (Paired, two-way ANOVA plus Šídák’s multiple comparisons test). ( right ) Quantification of residual tumor cells (CD45 - /GD2 + ) in the same samples. A total of 4 BMs were utilized and shown with different symbols. The degree of opacity indicates the E:T ratio utilized for each BM sample (10:1, 5:1 and 2.5:1; lower to higher opacity). The same E:T ratios were utilized for healthy donor blood NK-cells to facilitate comparison between groups. n ( left ) Representative contour plots of phagocytosis assay with GFP-labeled NB-EbC1 cells exposed to different cSNs or dinutuximab (10 µg/mL) together with macrophages. Macrophages alone are shown to define GFP + /CD11b + cells. ( right ) Quantification of NB-EbC1 phagocytosis. Means and SDs are shown ( n = 3 technical replicates). TM transmembrane, neg negative, cSN concentrated supernatant, BM bone marrow, HD healthy donor. Represented data has been validated with at least 2 independent experiments. Figure 3 a , f and g created with BioRender.com, and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International license. Source data are provided as a Source Data file.

    Journal: Nature Communications

    Article Title: CAR T-cell-mediated delivery of bispecific innate immune cell engagers for neuroblastoma

    doi: 10.1038/s41467-024-51337-2

    Figure Lengend Snippet: a Graphical illustration of T-cell GPC2.CAR expression and GD2.BiCE secretion. b Schematic representation of transgenes for two BiCE-secreting GPC2.CAR constructs targeting GD2 and CD19 (GPC2.CAR-GD2.BiCE and GPC2.CAR-CD19.BiCE, respectively), as well as single GPC2.CAR, CD19.CAR and GD2.BiCE constructs. c Detection of GD2 BiCE by western blot (His-tag) in cSN from HEK293T cells transfected with GPC2.CAR-GD2.BiCE vector. d Binding assays detecting secondary His-tag expression on tumor cells incubated with cSN from HEK293T cells transfected with different constructs as indicated. e Correlation between GD2 BiCE binding and GD2 cell surface expression in NB cell lines. Spearman correlation (two-tailed). f Illustration ( left ) and histograms ( right ) of binding assay evaluating human recombinant CD16a protein binding to tumor cells incubated with different CAR construct cSNs. g Illustration ( left ) and histograms ( right ) of binding assay evaluating 1A7 binding to human primary NK-cells or T-cells incubated with different CAR construct cSNs. 1, control medium; 2, GPC2.CAR; 3, GPC2.CAR-CD19.BiCE; and 4, GPC2.CAR-GD2.BiCE in ( d , f , and g ). h NK-cell-mediated specific lysis of NB-EbC1 cells in the presence of cSNs (5 ng/mL of His-tagged BiCE), or dinutuximab (10 µg/mL) as a positive control. * P = 0.0009 and ** P = 0.0028 (One-way ANOVA plus Tukey’s multiple comparison test). Means and SDs are shown ( n = 3 independent donors). i Co-expression of CD107a and CD69 by flow cytometry in NK-cells from the cytotoxicity experiment in ( h ). * P = 0.0003 (One-way ANOVA plus Tukey’s multiple comparison test). Means and SDs are shown ( n = 3 independent donors). j IFN-γ levels measured by ELISA in NK-cell supernatants from the cytotoxicity experiment in ( h ). * P = 0.0028 (One-way ANOVA plus Tukey’s multiple comparison test). Means and SDs are shown ( n = 3 independent donors). k Polyfunctionality pie charts indicating the percentage of single NK-cells secreting 1 or more cytokine when cultured alone or in the presence of NB-EbC1 cells together with GD2 BiCE, CD19 BiCE or dinutuximab as in ( h ). l NK92 WT vs. NK92-CD16a cell cytotoxicity against NB-EbC1 cells co-incubated with different cSNs or dinutuximab (10 µg/mL) as a positive control after 24 hours at a 10:1 E:T ratio. Means and SDs are shown (n = 3 technical replicates). m ( left ) Percentage of CD107a + NK-cells isolated from either neuroblastoma-infiltrating BM aspirates or peripheral blood of healthy donors after 24 hours of co-incubation with NB-EbC1 cells and cSNs (from GPC2.CAR-GD2.BiCE or GPC2.CAR-CD19.BiCE; 5 ng/mL). * P = 0.0139 and ** P < 0.0001 (Paired, two-way ANOVA plus Šídák’s multiple comparisons test). ( right ) Quantification of residual tumor cells (CD45 - /GD2 + ) in the same samples. A total of 4 BMs were utilized and shown with different symbols. The degree of opacity indicates the E:T ratio utilized for each BM sample (10:1, 5:1 and 2.5:1; lower to higher opacity). The same E:T ratios were utilized for healthy donor blood NK-cells to facilitate comparison between groups. n ( left ) Representative contour plots of phagocytosis assay with GFP-labeled NB-EbC1 cells exposed to different cSNs or dinutuximab (10 µg/mL) together with macrophages. Macrophages alone are shown to define GFP + /CD11b + cells. ( right ) Quantification of NB-EbC1 phagocytosis. Means and SDs are shown ( n = 3 technical replicates). TM transmembrane, neg negative, cSN concentrated supernatant, BM bone marrow, HD healthy donor. Represented data has been validated with at least 2 independent experiments. Figure 3 a , f and g created with BioRender.com, and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International license. Source data are provided as a Source Data file.

    Article Snippet: HEK293T and NK92-GFP-CD16 176V cell lines were obtained from ATCC (Catalog No. CRL-3216 and PTA-8836, respectively).

    Techniques: Expressing, Construct, Western Blot, Transfection, Plasmid Preparation, Binding Assay, Incubation, Two Tailed Test, Recombinant, Protein Binding, Control, Lysis, Positive Control, Comparison, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Cell Culture, Isolation, Phagocytosis Assay, Labeling

    a Schematic in vivo protocol for the biodistribution/pharmacokinetic study of GD2.BiCE compared to the GD2 antibody dinutuximab in mice. b GD2.BiCE levels (pg per mg of total tissue protein) in tumors and mouse normal tissues after CAR.BiCE T-cell infusion ( n = 13; except brainstem n = 12). Means and SDs are shown. **** P < 0.0001 (One-way ANOVA plus Dunnett’s multiple comparison test). c GD2 mAb levels (ng per mg of total tissue protein) in the same tissues as b , harvested at day 1 (circles), 2 (squares) and 3 (triangles) after the last dose of dinutuximab (tumor n = 9; spleen=10; lung, heart, cortex n = 11; remaining organs n = 12). Means and SDs are shown. * P = 0.016 and ** P = 0.025, # P = 0.0001, ## P < 0.0001 and ### P = 0.0040. (*; tumor vs. normal, # ; normal vs. tumor) (One-way ANOVA plus Dunnett’s multiple comparison test). d Quantification of human CD3-positive cells in IHC-stained samples from the biodistribution study in ( a ). Means and SEMs are shown ( n = 3). Circles, squares and triangles indicate 5, 6 and 7 day timepoints, respectively, after GPC2.CAR-GD2.BiCE T-cell infusion in ( b and d ). e CD3 IHC from tissues from a representative case from biodistribution assay of GPC2.CAR-GD2.BiCE T-cell-treated mice in ( a ). Scale bars are indicated. f Schematic in vivo protocol for the pharmacodynamics NK92 cell tumor accumulation study. g Serial IVIS imaging of mice bearing neuroblastoma PDXs after intratumoral NK92-CD16a-luc injection and intravenous infusion of GPC2.CAR-GD2.BiCE ( n = 5) or GPC2.CAR-CD19.BiCE T-cells ( n = 4). h ( left ) Serial quantification of NK92 cell retention in GPC2.CAR-GD2.BiCE and GPC2.CAR-CD19.BiCE-treated animals from g . Mean, SEM and substrate inhibition model curves are shown. ( right ) AUC 3-96h quantification from previous curves. Mean and SD are shown. * P = 0.015 (Mann–Whitney t -test). PDX patient-derived xenograft, ip intraperitoneal, iv intravenous, it intratumor, AUC area under the curve, luc luciferase, h hours. Source data are provided as a Source Data file.

    Journal: Nature Communications

    Article Title: CAR T-cell-mediated delivery of bispecific innate immune cell engagers for neuroblastoma

    doi: 10.1038/s41467-024-51337-2

    Figure Lengend Snippet: a Schematic in vivo protocol for the biodistribution/pharmacokinetic study of GD2.BiCE compared to the GD2 antibody dinutuximab in mice. b GD2.BiCE levels (pg per mg of total tissue protein) in tumors and mouse normal tissues after CAR.BiCE T-cell infusion ( n = 13; except brainstem n = 12). Means and SDs are shown. **** P < 0.0001 (One-way ANOVA plus Dunnett’s multiple comparison test). c GD2 mAb levels (ng per mg of total tissue protein) in the same tissues as b , harvested at day 1 (circles), 2 (squares) and 3 (triangles) after the last dose of dinutuximab (tumor n = 9; spleen=10; lung, heart, cortex n = 11; remaining organs n = 12). Means and SDs are shown. * P = 0.016 and ** P = 0.025, # P = 0.0001, ## P < 0.0001 and ### P = 0.0040. (*; tumor vs. normal, # ; normal vs. tumor) (One-way ANOVA plus Dunnett’s multiple comparison test). d Quantification of human CD3-positive cells in IHC-stained samples from the biodistribution study in ( a ). Means and SEMs are shown ( n = 3). Circles, squares and triangles indicate 5, 6 and 7 day timepoints, respectively, after GPC2.CAR-GD2.BiCE T-cell infusion in ( b and d ). e CD3 IHC from tissues from a representative case from biodistribution assay of GPC2.CAR-GD2.BiCE T-cell-treated mice in ( a ). Scale bars are indicated. f Schematic in vivo protocol for the pharmacodynamics NK92 cell tumor accumulation study. g Serial IVIS imaging of mice bearing neuroblastoma PDXs after intratumoral NK92-CD16a-luc injection and intravenous infusion of GPC2.CAR-GD2.BiCE ( n = 5) or GPC2.CAR-CD19.BiCE T-cells ( n = 4). h ( left ) Serial quantification of NK92 cell retention in GPC2.CAR-GD2.BiCE and GPC2.CAR-CD19.BiCE-treated animals from g . Mean, SEM and substrate inhibition model curves are shown. ( right ) AUC 3-96h quantification from previous curves. Mean and SD are shown. * P = 0.015 (Mann–Whitney t -test). PDX patient-derived xenograft, ip intraperitoneal, iv intravenous, it intratumor, AUC area under the curve, luc luciferase, h hours. Source data are provided as a Source Data file.

    Article Snippet: HEK293T and NK92-GFP-CD16 176V cell lines were obtained from ATCC (Catalog No. CRL-3216 and PTA-8836, respectively).

    Techniques: In Vivo, Comparison, Staining, Imaging, Injection, Inhibition, MANN-WHITNEY, Derivative Assay, Luciferase