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mouse apoe elisa pro kit  (Mabtech Inc)

 
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    Mabtech Inc mouse apoe elisa pro kit
    <t>ApoE</t> is the most highly expressed immune suppressive gene in the melanoma B16-F10 cell lines and apoE serum levels rise with tumor growth in vivo. (A) mRNA expression as revealed by nanostring nsolver Pancancer immune profiling, of the immune suppressive marker genes in B16F10 cells (n=6). (B) ApoE expression was undetectable in the serum of apoE knockout (apoE-/-) mice, but present at high levels in wild type (C57/BL6) mice with <t>ELISA</t> assay. (C) ApoE knockout mice were inoculated with 10^4 wild type (B16F10) cells and serum levels of apoE increased over time with increasing tumor size. (D) Validation of apoE gene knockout in B16F10 cells by CRISPR-Cas9 gene deletion. The level of apoE protein expression was measured in WT B16F10 and the corresponding apoE-/- clone by Western Blot. (E) Equivalent numbers of WT and apoE-/- B16 cells were plated and apoE levels released into culture media were quantified by ELISA at 48hr. ApoE is secreted at high levels in WT B16 cells and is not detectable in the apoE-/- cell line. (F) To evaluate whether targeting apoE influenced cell viability and proliferation, 5x10^4 WT (n=6) or apoE-/- B16 cells (n=6) were grown in 12-well plates and proliferation rates were measured at 24hr and 48hr by MTT assay. There is no statistically significant difference in cell proliferation rate between the two groups. (G) Cell cycle distribution was determined in WT and apoE-/- B16 cells. The various phases of the cell cycle are differentiated in the flow cytometry plot on the left: G0-G1 is the pre-synthesis phase, S-phase cells are undergoing active DNA synthesis and G2-M cells are preparing for mitosis. Bar graphs represents the percentage of cells in G0-G1, S and M phase of the cell cycle. Cell counts and cell cycle distribution indicate that WT and apoE-/- B16 cells proliferate at equivalent rates. Data are representative of three independent experiments. Results are expressed as mean score ±SD. ***p<0.001, determined by unpaired two-tailed Student’s t-test.
    Mouse Apoe Elisa Pro Kit, supplied by Mabtech Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse apoe elisa pro kit/product/Mabtech Inc
    Average 90 stars, based on 1 article reviews
    mouse apoe elisa pro kit - by Bioz Stars, 2026-03
    90/100 stars

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    1) Product Images from "Tumor Apolipoprotein E is a key checkpoint blocking anti-tumor immunity in mouse melanoma"

    Article Title: Tumor Apolipoprotein E is a key checkpoint blocking anti-tumor immunity in mouse melanoma

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2022.991790

    ApoE is the most highly expressed immune suppressive gene in the melanoma B16-F10 cell lines and apoE serum levels rise with tumor growth in vivo. (A) mRNA expression as revealed by nanostring nsolver Pancancer immune profiling, of the immune suppressive marker genes in B16F10 cells (n=6). (B) ApoE expression was undetectable in the serum of apoE knockout (apoE-/-) mice, but present at high levels in wild type (C57/BL6) mice with ELISA assay. (C) ApoE knockout mice were inoculated with 10^4 wild type (B16F10) cells and serum levels of apoE increased over time with increasing tumor size. (D) Validation of apoE gene knockout in B16F10 cells by CRISPR-Cas9 gene deletion. The level of apoE protein expression was measured in WT B16F10 and the corresponding apoE-/- clone by Western Blot. (E) Equivalent numbers of WT and apoE-/- B16 cells were plated and apoE levels released into culture media were quantified by ELISA at 48hr. ApoE is secreted at high levels in WT B16 cells and is not detectable in the apoE-/- cell line. (F) To evaluate whether targeting apoE influenced cell viability and proliferation, 5x10^4 WT (n=6) or apoE-/- B16 cells (n=6) were grown in 12-well plates and proliferation rates were measured at 24hr and 48hr by MTT assay. There is no statistically significant difference in cell proliferation rate between the two groups. (G) Cell cycle distribution was determined in WT and apoE-/- B16 cells. The various phases of the cell cycle are differentiated in the flow cytometry plot on the left: G0-G1 is the pre-synthesis phase, S-phase cells are undergoing active DNA synthesis and G2-M cells are preparing for mitosis. Bar graphs represents the percentage of cells in G0-G1, S and M phase of the cell cycle. Cell counts and cell cycle distribution indicate that WT and apoE-/- B16 cells proliferate at equivalent rates. Data are representative of three independent experiments. Results are expressed as mean score ±SD. ***p<0.001, determined by unpaired two-tailed Student’s t-test.
    Figure Legend Snippet: ApoE is the most highly expressed immune suppressive gene in the melanoma B16-F10 cell lines and apoE serum levels rise with tumor growth in vivo. (A) mRNA expression as revealed by nanostring nsolver Pancancer immune profiling, of the immune suppressive marker genes in B16F10 cells (n=6). (B) ApoE expression was undetectable in the serum of apoE knockout (apoE-/-) mice, but present at high levels in wild type (C57/BL6) mice with ELISA assay. (C) ApoE knockout mice were inoculated with 10^4 wild type (B16F10) cells and serum levels of apoE increased over time with increasing tumor size. (D) Validation of apoE gene knockout in B16F10 cells by CRISPR-Cas9 gene deletion. The level of apoE protein expression was measured in WT B16F10 and the corresponding apoE-/- clone by Western Blot. (E) Equivalent numbers of WT and apoE-/- B16 cells were plated and apoE levels released into culture media were quantified by ELISA at 48hr. ApoE is secreted at high levels in WT B16 cells and is not detectable in the apoE-/- cell line. (F) To evaluate whether targeting apoE influenced cell viability and proliferation, 5x10^4 WT (n=6) or apoE-/- B16 cells (n=6) were grown in 12-well plates and proliferation rates were measured at 24hr and 48hr by MTT assay. There is no statistically significant difference in cell proliferation rate between the two groups. (G) Cell cycle distribution was determined in WT and apoE-/- B16 cells. The various phases of the cell cycle are differentiated in the flow cytometry plot on the left: G0-G1 is the pre-synthesis phase, S-phase cells are undergoing active DNA synthesis and G2-M cells are preparing for mitosis. Bar graphs represents the percentage of cells in G0-G1, S and M phase of the cell cycle. Cell counts and cell cycle distribution indicate that WT and apoE-/- B16 cells proliferate at equivalent rates. Data are representative of three independent experiments. Results are expressed as mean score ±SD. ***p<0.001, determined by unpaired two-tailed Student’s t-test.

    Techniques Used: In Vivo, Expressing, Marker, Knock-Out, Enzyme-linked Immunosorbent Assay, Biomarker Discovery, Gene Knockout, CRISPR, Western Blot, MTT Assay, Flow Cytometry, DNA Synthesis, Two Tailed Test

    ApoE secreted into media from B16 melanoma tumor cells inhibits T-cell proliferation and function. (A) Conditioned media (CM) from WT or apoE -/- cells was cultured with T-cells activated by CD3/CD28 beads. Bar graphs depict IFNγ released under these conditions. The production of IFNγ was significantly suppressed when T cells were cultured in WT B16 CM, but this suppression was reversed in apoE free CM from apoE -/- cells. (B) Representative flow cytometry plots and (C) quantification of T cell apoptosis in CM. Results show that T cell viability is markedly reduced in the WT CM, whereas induction of apoptosis was reversed when cells were cultured in the apoE -/- medium, similar to RPMI control medium alone. (D) Representative flow cytometry plots and (E) quantification of cell cycle analysis of T cells in different media. Cell cycle distribution showed an arrest of activated T cells in the G0-G1 phase in the WT B16 medium, while in the apoE -/- medium most T cells were distributed in the S and G2-M phases, similar to the RPMI media control. Results are expressed as mean score ± SD. *p<0.05; **p<0.005; ***p<0.001, determined by unpaired two-tailed Student’s t-test.
    Figure Legend Snippet: ApoE secreted into media from B16 melanoma tumor cells inhibits T-cell proliferation and function. (A) Conditioned media (CM) from WT or apoE -/- cells was cultured with T-cells activated by CD3/CD28 beads. Bar graphs depict IFNγ released under these conditions. The production of IFNγ was significantly suppressed when T cells were cultured in WT B16 CM, but this suppression was reversed in apoE free CM from apoE -/- cells. (B) Representative flow cytometry plots and (C) quantification of T cell apoptosis in CM. Results show that T cell viability is markedly reduced in the WT CM, whereas induction of apoptosis was reversed when cells were cultured in the apoE -/- medium, similar to RPMI control medium alone. (D) Representative flow cytometry plots and (E) quantification of cell cycle analysis of T cells in different media. Cell cycle distribution showed an arrest of activated T cells in the G0-G1 phase in the WT B16 medium, while in the apoE -/- medium most T cells were distributed in the S and G2-M phases, similar to the RPMI media control. Results are expressed as mean score ± SD. *p<0.05; **p<0.005; ***p<0.001, determined by unpaired two-tailed Student’s t-test.

    Techniques Used: Cell Culture, Flow Cytometry, Control, Cell Cycle Assay, Two Tailed Test

    ApoE agonist peptide COG133 inhibits cytokine secretion induced by immunogenic tumor cells, while anti-APOE blocking antibody enhances cytokine secretion in tumor cell/splenocyte reactions. (A) Naïve and vaccinated splenocyte production of IFNγ was markedly reduced when splenocytes were co-cultured with immunogenic (BET/JQ1 treated) B16 tumor cells in the presence of the apoE agonist COG133. (B) Naïve splenocyte production of IFNγ was significantly increased when co-cultured with immunogenic B16 tumor cells with anti-APOE antibody. (C) . COG133 was also inhibitory of IFNγ production when vaccinated splenocytes were used for co-culture with treated immunogenic cancer cells. It is of interest to note that the levels of IFNγ production is significantly greater when vaccinated splenocytes were used for this experiment. NS: naïve splenocytes, splenocytes were collected from naïve C57BL/6 mice. Treated B16: B16 cells were expose to Myc inhibitor (0.25µM BET and 0.25µM JQ1) for 4 days, to induce immunogenicity. VS: vaccinated splenocytes. Irradiated 10 4 WT B16 tumor cells and 100ug/ml anti-CTLA4 antibody were administered to C57BL/6 mice on day 0, and splenocytes were collected at day 7 after tumor cell inoculation. Data are representative of three independent experiments. Results are expressed as mean score ± SD. *p<0.05; **p<0.005; ***p<0.001, determined by unpaired two-tailed Student’s t-test.
    Figure Legend Snippet: ApoE agonist peptide COG133 inhibits cytokine secretion induced by immunogenic tumor cells, while anti-APOE blocking antibody enhances cytokine secretion in tumor cell/splenocyte reactions. (A) Naïve and vaccinated splenocyte production of IFNγ was markedly reduced when splenocytes were co-cultured with immunogenic (BET/JQ1 treated) B16 tumor cells in the presence of the apoE agonist COG133. (B) Naïve splenocyte production of IFNγ was significantly increased when co-cultured with immunogenic B16 tumor cells with anti-APOE antibody. (C) . COG133 was also inhibitory of IFNγ production when vaccinated splenocytes were used for co-culture with treated immunogenic cancer cells. It is of interest to note that the levels of IFNγ production is significantly greater when vaccinated splenocytes were used for this experiment. NS: naïve splenocytes, splenocytes were collected from naïve C57BL/6 mice. Treated B16: B16 cells were expose to Myc inhibitor (0.25µM BET and 0.25µM JQ1) for 4 days, to induce immunogenicity. VS: vaccinated splenocytes. Irradiated 10 4 WT B16 tumor cells and 100ug/ml anti-CTLA4 antibody were administered to C57BL/6 mice on day 0, and splenocytes were collected at day 7 after tumor cell inoculation. Data are representative of three independent experiments. Results are expressed as mean score ± SD. *p<0.05; **p<0.005; ***p<0.001, determined by unpaired two-tailed Student’s t-test.

    Techniques Used: Blocking Assay, Cell Culture, Co-Culture Assay, Immunopeptidomics, Irradiation, Two Tailed Test

    lrp8 is the most dominant receptor expressed on activated T cells and blocking lrp8 enhanced T-cell activation. (A) Expression of apoE receptors shows predominance of ldlr and lrp8 receptors on T cells, (B) lrp8, ldl and lrp1 receptors on dendritic cells, and (C) lrp1 receptors on macrophages as shown by quantitative real-time PCR (qPCR). Expression of ldlr and lrp8 was upregulated following T cell stimulation with CD3/CD28 beads. Expression of lrp8 was also upregulated following dendritic cell stimulation with TLR7/8. (D) The amount of IFNγ production from vaccinated splenocytes co-cultured with immunogenic WT B16 cells was quantified by ELISA assay. Results show that IFNγ production was significantly suppressed in the presence of the apoE agonist COG133, but suppression did not occur when splenocytes were harvested from lrp8 -/- mice. These findings suggest that T-cell function is at least partially inhibited by apoE through the lrp8 receptor pathway. Results are expressed as mean score ± SD. *p<0.05; **p<0.005; ***p<0.001, determined by unpaired two-tailed Student’s t-test.
    Figure Legend Snippet: lrp8 is the most dominant receptor expressed on activated T cells and blocking lrp8 enhanced T-cell activation. (A) Expression of apoE receptors shows predominance of ldlr and lrp8 receptors on T cells, (B) lrp8, ldl and lrp1 receptors on dendritic cells, and (C) lrp1 receptors on macrophages as shown by quantitative real-time PCR (qPCR). Expression of ldlr and lrp8 was upregulated following T cell stimulation with CD3/CD28 beads. Expression of lrp8 was also upregulated following dendritic cell stimulation with TLR7/8. (D) The amount of IFNγ production from vaccinated splenocytes co-cultured with immunogenic WT B16 cells was quantified by ELISA assay. Results show that IFNγ production was significantly suppressed in the presence of the apoE agonist COG133, but suppression did not occur when splenocytes were harvested from lrp8 -/- mice. These findings suggest that T-cell function is at least partially inhibited by apoE through the lrp8 receptor pathway. Results are expressed as mean score ± SD. *p<0.05; **p<0.005; ***p<0.001, determined by unpaired two-tailed Student’s t-test.

    Techniques Used: Blocking Assay, Activation Assay, Expressing, Real-time Polymerase Chain Reaction, Cell Stimulation, Cell Culture, Enzyme-linked Immunosorbent Assay, Cell Function Assay, Two Tailed Test

    Knock out of apoE in both B16 tumor cells and in mice enhances host immunity and attenuates tumorigenicity. (A) In vivo, 104 WT or apoE-/- B16 cells were injected into the right leg of WT (n=9), apoE-/- (n=9) or lrp8-/- mice (n=9). The average tumor growth in each group (n=6) is compared. Tumor growth was significantly slower when apoE-/- B16 cells were injected into apoE-/- or lrp8-/- mice versus the other groups (two-way ANOVA; P <0.0001). (B) The final tumor volume between treatment groups at the end point of the experiment (Day 20) was also compared using a one-way ANOVA followed by Tukey HSD pairwise multiple comparisons between treatment groups. Tumor volumes at the end point of the experiment were significantly different between treatment groups (one-way ANOVA; P <0.0001). *p<0.05; **p<0.01; ****p<0.0001.
    Figure Legend Snippet: Knock out of apoE in both B16 tumor cells and in mice enhances host immunity and attenuates tumorigenicity. (A) In vivo, 104 WT or apoE-/- B16 cells were injected into the right leg of WT (n=9), apoE-/- (n=9) or lrp8-/- mice (n=9). The average tumor growth in each group (n=6) is compared. Tumor growth was significantly slower when apoE-/- B16 cells were injected into apoE-/- or lrp8-/- mice versus the other groups (two-way ANOVA; P <0.0001). (B) The final tumor volume between treatment groups at the end point of the experiment (Day 20) was also compared using a one-way ANOVA followed by Tukey HSD pairwise multiple comparisons between treatment groups. Tumor volumes at the end point of the experiment were significantly different between treatment groups (one-way ANOVA; P <0.0001). *p<0.05; **p<0.01; ****p<0.0001.

    Techniques Used: Knock-Out, In Vivo, Injection

    Survival curve (A) Survival was significantly better (n=9) when apoE -/- B16 cells were injected into apoE -/- or lrp8 -/- mice versus the other groups. (B) The median survival time and the cumulative survival probability were calculated and compared using the Kaplan-Meier survival estimator followed by a log-rank test, and the hazard ratio (HR) was calculated using the Cox proportional-hazards regression model. The comparison between the groups is shown in the table.
    Figure Legend Snippet: Survival curve (A) Survival was significantly better (n=9) when apoE -/- B16 cells were injected into apoE -/- or lrp8 -/- mice versus the other groups. (B) The median survival time and the cumulative survival probability were calculated and compared using the Kaplan-Meier survival estimator followed by a log-rank test, and the hazard ratio (HR) was calculated using the Cox proportional-hazards regression model. The comparison between the groups is shown in the table.

    Techniques Used: Injection, Comparison

    The first three tumors that reached 15mm in each of the experimental groups were harvested and the immune cell infiltrate and immune pathway activation was analyzed with nanostring Pancancer immune profiling. (A) Immune cell type scores and (B) immune pathway (signature) scores show that immune cell infiltrates and immune pathway activation were greatest when apoE-/- cells were injected into apoE-/- mice. Dot line plots show the score trends of 12 immune cell lines and 29 immune pathways. Box plots show selective representative score comparisons. Results are expressed as mean score ±SD. *p<0.05, determined by unpaired two-tailed Student’s t-test. Wt/wt: wt B16 cells injected in wt mice; apoE-/-/apoE-/-: apoE-/- cells injected in apoE-/- mice; apoE-/-/lrp8-/-: apoE-/- cells injected in lrp8-/- mice; apoE-/-/wt: apoE-/- cells injected in wt mice; wt/apoE-/-: wt cells injected in apoE-/- mice; wt//lrp8-/-: wt cells injected in lrp8-/- mice.
    Figure Legend Snippet: The first three tumors that reached 15mm in each of the experimental groups were harvested and the immune cell infiltrate and immune pathway activation was analyzed with nanostring Pancancer immune profiling. (A) Immune cell type scores and (B) immune pathway (signature) scores show that immune cell infiltrates and immune pathway activation were greatest when apoE-/- cells were injected into apoE-/- mice. Dot line plots show the score trends of 12 immune cell lines and 29 immune pathways. Box plots show selective representative score comparisons. Results are expressed as mean score ±SD. *p<0.05, determined by unpaired two-tailed Student’s t-test. Wt/wt: wt B16 cells injected in wt mice; apoE-/-/apoE-/-: apoE-/- cells injected in apoE-/- mice; apoE-/-/lrp8-/-: apoE-/- cells injected in lrp8-/- mice; apoE-/-/wt: apoE-/- cells injected in wt mice; wt/apoE-/-: wt cells injected in apoE-/- mice; wt//lrp8-/-: wt cells injected in lrp8-/- mice.

    Techniques Used: Activation Assay, Injection, Two Tailed Test

    Nanostring PanCancer Immune Profiling analysis of RNAseq of activation markers for T cells and DCs that infiltrated into the tumors from the 6 different groups. (A) Activated T cell genes and (B) activated DC genes were all statistically significantly increased in the tumor from apoE-/-/apoE-/- group when compared with wt/wt control groups. The relative gene expression level was indicated on the y-axis and tumor groups are listed along the x-axis. Results are expressed as mean score ±SE. *p<0.05, determined by unpaired two-tailed Student’s t-test.
    Figure Legend Snippet: Nanostring PanCancer Immune Profiling analysis of RNAseq of activation markers for T cells and DCs that infiltrated into the tumors from the 6 different groups. (A) Activated T cell genes and (B) activated DC genes were all statistically significantly increased in the tumor from apoE-/-/apoE-/- group when compared with wt/wt control groups. The relative gene expression level was indicated on the y-axis and tumor groups are listed along the x-axis. Results are expressed as mean score ±SE. *p<0.05, determined by unpaired two-tailed Student’s t-test.

    Techniques Used: Activation Assay, Control, Gene Expression, Two Tailed Test

    To validate nanostring results, both CD45 and CD3 expression were examined with IHC staining in the tumors from WT or apoE-/- mice following injection with WT or apoE-/- tumor cells. Representative images of CD45 (A) and CD3 (C) staining visualized with DAB (brown) and counterstained with hematoxylin (blue, nuclei). (B, D) Optical density (mean gray value) obtained by color deconvolution analysis. Optical density graph bars represent the mean ± SD (n = 30 images). ***p<0.001, determined by unpaired two-tailed Student’s t-test. Wt/wt: wt B16 cells injected in wt mice; apoE-/- /apoE-/-: apoE-/- cells injected in apoE-/- mice.
    Figure Legend Snippet: To validate nanostring results, both CD45 and CD3 expression were examined with IHC staining in the tumors from WT or apoE-/- mice following injection with WT or apoE-/- tumor cells. Representative images of CD45 (A) and CD3 (C) staining visualized with DAB (brown) and counterstained with hematoxylin (blue, nuclei). (B, D) Optical density (mean gray value) obtained by color deconvolution analysis. Optical density graph bars represent the mean ± SD (n = 30 images). ***p<0.001, determined by unpaired two-tailed Student’s t-test. Wt/wt: wt B16 cells injected in wt mice; apoE-/- /apoE-/-: apoE-/- cells injected in apoE-/- mice.

    Techniques Used: Expressing, Immunohistochemistry, Injection, Staining, Two Tailed Test

    ApoE knock out in B16 tumor cells induces potent immunogenicity. Wild type and apoE -/- mice (A) or wild type and lrp8 -/- mice (B) , were inoculated with either WT B16 or apoE -/- cells, with anti-CTLA4 antibody on day 0. Splenocytes were harvested on day 7 and co-cultured with either WT B16 or apoE -/- B16 cells for 48hr, following which IFNγ levels in media were compared with ELISA assay. Results show that IFNγ production is highest for all groups when apoE -/- cells are used. These findings re-iterate the potent inhibitory effect of apoE on immune cell activation in the cancer environment. Results are expressed as mean score ± SD. *p<0.05; **p<0.005; ***p<0.001, determined by unpaired two-tailed Student’s t-test.
    Figure Legend Snippet: ApoE knock out in B16 tumor cells induces potent immunogenicity. Wild type and apoE -/- mice (A) or wild type and lrp8 -/- mice (B) , were inoculated with either WT B16 or apoE -/- cells, with anti-CTLA4 antibody on day 0. Splenocytes were harvested on day 7 and co-cultured with either WT B16 or apoE -/- B16 cells for 48hr, following which IFNγ levels in media were compared with ELISA assay. Results show that IFNγ production is highest for all groups when apoE -/- cells are used. These findings re-iterate the potent inhibitory effect of apoE on immune cell activation in the cancer environment. Results are expressed as mean score ± SD. *p<0.05; **p<0.005; ***p<0.001, determined by unpaired two-tailed Student’s t-test.

    Techniques Used: Knock-Out, Immunopeptidomics, Cell Culture, Enzyme-linked Immunosorbent Assay, Activation Assay, Two Tailed Test

    ApoE RNA-seq expression is abundant in cutaneous melanoma but is not associated with PD-L1 or PD1. Scatterplots showing mRNA expression correlation of APOE (x-axis) with PD-L1, PD1 and APOC1 from the TCGA melanoma datasets based on their RNA-seq gene expression values (measured by RSEM algorithm). APOE expression did not correlate with PD-L1 or PD1 but did positively correlate with APOC1 expression which was used as a control gene. The correlation was evaluated by the Spearman correlation coefficient with a cut-off value of 0.5 and P-value used a cut-off value of 0.05.
    Figure Legend Snippet: ApoE RNA-seq expression is abundant in cutaneous melanoma but is not associated with PD-L1 or PD1. Scatterplots showing mRNA expression correlation of APOE (x-axis) with PD-L1, PD1 and APOC1 from the TCGA melanoma datasets based on their RNA-seq gene expression values (measured by RSEM algorithm). APOE expression did not correlate with PD-L1 or PD1 but did positively correlate with APOC1 expression which was used as a control gene. The correlation was evaluated by the Spearman correlation coefficient with a cut-off value of 0.5 and P-value used a cut-off value of 0.05.

    Techniques Used: RNA Sequencing, Expressing, Gene Expression, Control

    Scatterplots show the tumor purity-corrected partial Spearman’s rho value and the correlation between gene expression with infiltration of six immune cell estimates. Top row is APOE expression while the bottom row depicts PD-L1. PD-L1 correlated with CD8 T cell and neutrophil infiltrates, while APOE does not correlate with immune cell infiltrates. The correlation was evaluated by the Spearman correlation coefficient with a cut-off value of 0.5 and P-value used a cut-off value of 0.05.
    Figure Legend Snippet: Scatterplots show the tumor purity-corrected partial Spearman’s rho value and the correlation between gene expression with infiltration of six immune cell estimates. Top row is APOE expression while the bottom row depicts PD-L1. PD-L1 correlated with CD8 T cell and neutrophil infiltrates, while APOE does not correlate with immune cell infiltrates. The correlation was evaluated by the Spearman correlation coefficient with a cut-off value of 0.5 and P-value used a cut-off value of 0.05.

    Techniques Used: Gene Expression, Expressing

    Cumulative survival of patients associated with bifurcate gene expression at 30%. TCGA database includes primary and metastasis samples (n=462). APOE expression did not associate with survival, while PD-L1 and PD1 was associated with survival at this level of analysis. The correlation was evaluated by the Spearman correlation coefficient with a cut-off value of 0.5 and P-value used a cut-off value of 0.05.
    Figure Legend Snippet: Cumulative survival of patients associated with bifurcate gene expression at 30%. TCGA database includes primary and metastasis samples (n=462). APOE expression did not associate with survival, while PD-L1 and PD1 was associated with survival at this level of analysis. The correlation was evaluated by the Spearman correlation coefficient with a cut-off value of 0.5 and P-value used a cut-off value of 0.05.

    Techniques Used: Gene Expression, Expressing



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    Mabtech Inc mouse apoe elisa pro kit
    <t>ApoE</t> is the most highly expressed immune suppressive gene in the melanoma B16-F10 cell lines and apoE serum levels rise with tumor growth in vivo. (A) mRNA expression as revealed by nanostring nsolver Pancancer immune profiling, of the immune suppressive marker genes in B16F10 cells (n=6). (B) ApoE expression was undetectable in the serum of apoE knockout (apoE-/-) mice, but present at high levels in wild type (C57/BL6) mice with <t>ELISA</t> assay. (C) ApoE knockout mice were inoculated with 10^4 wild type (B16F10) cells and serum levels of apoE increased over time with increasing tumor size. (D) Validation of apoE gene knockout in B16F10 cells by CRISPR-Cas9 gene deletion. The level of apoE protein expression was measured in WT B16F10 and the corresponding apoE-/- clone by Western Blot. (E) Equivalent numbers of WT and apoE-/- B16 cells were plated and apoE levels released into culture media were quantified by ELISA at 48hr. ApoE is secreted at high levels in WT B16 cells and is not detectable in the apoE-/- cell line. (F) To evaluate whether targeting apoE influenced cell viability and proliferation, 5x10^4 WT (n=6) or apoE-/- B16 cells (n=6) were grown in 12-well plates and proliferation rates were measured at 24hr and 48hr by MTT assay. There is no statistically significant difference in cell proliferation rate between the two groups. (G) Cell cycle distribution was determined in WT and apoE-/- B16 cells. The various phases of the cell cycle are differentiated in the flow cytometry plot on the left: G0-G1 is the pre-synthesis phase, S-phase cells are undergoing active DNA synthesis and G2-M cells are preparing for mitosis. Bar graphs represents the percentage of cells in G0-G1, S and M phase of the cell cycle. Cell counts and cell cycle distribution indicate that WT and apoE-/- B16 cells proliferate at equivalent rates. Data are representative of three independent experiments. Results are expressed as mean score ±SD. ***p<0.001, determined by unpaired two-tailed Student’s t-test.
    Mouse Apoe Elisa Pro Kit, supplied by Mabtech Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ApoE is the most highly expressed immune suppressive gene in the melanoma B16-F10 cell lines and apoE serum levels rise with tumor growth in vivo. (A) mRNA expression as revealed by nanostring nsolver Pancancer immune profiling, of the immune suppressive marker genes in B16F10 cells (n=6). (B) ApoE expression was undetectable in the serum of apoE knockout (apoE-/-) mice, but present at high levels in wild type (C57/BL6) mice with ELISA assay. (C) ApoE knockout mice were inoculated with 10^4 wild type (B16F10) cells and serum levels of apoE increased over time with increasing tumor size. (D) Validation of apoE gene knockout in B16F10 cells by CRISPR-Cas9 gene deletion. The level of apoE protein expression was measured in WT B16F10 and the corresponding apoE-/- clone by Western Blot. (E) Equivalent numbers of WT and apoE-/- B16 cells were plated and apoE levels released into culture media were quantified by ELISA at 48hr. ApoE is secreted at high levels in WT B16 cells and is not detectable in the apoE-/- cell line. (F) To evaluate whether targeting apoE influenced cell viability and proliferation, 5x10^4 WT (n=6) or apoE-/- B16 cells (n=6) were grown in 12-well plates and proliferation rates were measured at 24hr and 48hr by MTT assay. There is no statistically significant difference in cell proliferation rate between the two groups. (G) Cell cycle distribution was determined in WT and apoE-/- B16 cells. The various phases of the cell cycle are differentiated in the flow cytometry plot on the left: G0-G1 is the pre-synthesis phase, S-phase cells are undergoing active DNA synthesis and G2-M cells are preparing for mitosis. Bar graphs represents the percentage of cells in G0-G1, S and M phase of the cell cycle. Cell counts and cell cycle distribution indicate that WT and apoE-/- B16 cells proliferate at equivalent rates. Data are representative of three independent experiments. Results are expressed as mean score ±SD. ***p<0.001, determined by unpaired two-tailed Student’s t-test.

    Journal: Frontiers in Immunology

    Article Title: Tumor Apolipoprotein E is a key checkpoint blocking anti-tumor immunity in mouse melanoma

    doi: 10.3389/fimmu.2022.991790

    Figure Lengend Snippet: ApoE is the most highly expressed immune suppressive gene in the melanoma B16-F10 cell lines and apoE serum levels rise with tumor growth in vivo. (A) mRNA expression as revealed by nanostring nsolver Pancancer immune profiling, of the immune suppressive marker genes in B16F10 cells (n=6). (B) ApoE expression was undetectable in the serum of apoE knockout (apoE-/-) mice, but present at high levels in wild type (C57/BL6) mice with ELISA assay. (C) ApoE knockout mice were inoculated with 10^4 wild type (B16F10) cells and serum levels of apoE increased over time with increasing tumor size. (D) Validation of apoE gene knockout in B16F10 cells by CRISPR-Cas9 gene deletion. The level of apoE protein expression was measured in WT B16F10 and the corresponding apoE-/- clone by Western Blot. (E) Equivalent numbers of WT and apoE-/- B16 cells were plated and apoE levels released into culture media were quantified by ELISA at 48hr. ApoE is secreted at high levels in WT B16 cells and is not detectable in the apoE-/- cell line. (F) To evaluate whether targeting apoE influenced cell viability and proliferation, 5x10^4 WT (n=6) or apoE-/- B16 cells (n=6) were grown in 12-well plates and proliferation rates were measured at 24hr and 48hr by MTT assay. There is no statistically significant difference in cell proliferation rate between the two groups. (G) Cell cycle distribution was determined in WT and apoE-/- B16 cells. The various phases of the cell cycle are differentiated in the flow cytometry plot on the left: G0-G1 is the pre-synthesis phase, S-phase cells are undergoing active DNA synthesis and G2-M cells are preparing for mitosis. Bar graphs represents the percentage of cells in G0-G1, S and M phase of the cell cycle. Cell counts and cell cycle distribution indicate that WT and apoE-/- B16 cells proliferate at equivalent rates. Data are representative of three independent experiments. Results are expressed as mean score ±SD. ***p<0.001, determined by unpaired two-tailed Student’s t-test.

    Article Snippet: ApoE levels in mouse sera were quantified using the mouse apoE ELISA PRO kit from Mabtech (Cincinnati, OH) as per the manufacturer’s directions.

    Techniques: In Vivo, Expressing, Marker, Knock-Out, Enzyme-linked Immunosorbent Assay, Biomarker Discovery, Gene Knockout, CRISPR, Western Blot, MTT Assay, Flow Cytometry, DNA Synthesis, Two Tailed Test

    ApoE secreted into media from B16 melanoma tumor cells inhibits T-cell proliferation and function. (A) Conditioned media (CM) from WT or apoE -/- cells was cultured with T-cells activated by CD3/CD28 beads. Bar graphs depict IFNγ released under these conditions. The production of IFNγ was significantly suppressed when T cells were cultured in WT B16 CM, but this suppression was reversed in apoE free CM from apoE -/- cells. (B) Representative flow cytometry plots and (C) quantification of T cell apoptosis in CM. Results show that T cell viability is markedly reduced in the WT CM, whereas induction of apoptosis was reversed when cells were cultured in the apoE -/- medium, similar to RPMI control medium alone. (D) Representative flow cytometry plots and (E) quantification of cell cycle analysis of T cells in different media. Cell cycle distribution showed an arrest of activated T cells in the G0-G1 phase in the WT B16 medium, while in the apoE -/- medium most T cells were distributed in the S and G2-M phases, similar to the RPMI media control. Results are expressed as mean score ± SD. *p<0.05; **p<0.005; ***p<0.001, determined by unpaired two-tailed Student’s t-test.

    Journal: Frontiers in Immunology

    Article Title: Tumor Apolipoprotein E is a key checkpoint blocking anti-tumor immunity in mouse melanoma

    doi: 10.3389/fimmu.2022.991790

    Figure Lengend Snippet: ApoE secreted into media from B16 melanoma tumor cells inhibits T-cell proliferation and function. (A) Conditioned media (CM) from WT or apoE -/- cells was cultured with T-cells activated by CD3/CD28 beads. Bar graphs depict IFNγ released under these conditions. The production of IFNγ was significantly suppressed when T cells were cultured in WT B16 CM, but this suppression was reversed in apoE free CM from apoE -/- cells. (B) Representative flow cytometry plots and (C) quantification of T cell apoptosis in CM. Results show that T cell viability is markedly reduced in the WT CM, whereas induction of apoptosis was reversed when cells were cultured in the apoE -/- medium, similar to RPMI control medium alone. (D) Representative flow cytometry plots and (E) quantification of cell cycle analysis of T cells in different media. Cell cycle distribution showed an arrest of activated T cells in the G0-G1 phase in the WT B16 medium, while in the apoE -/- medium most T cells were distributed in the S and G2-M phases, similar to the RPMI media control. Results are expressed as mean score ± SD. *p<0.05; **p<0.005; ***p<0.001, determined by unpaired two-tailed Student’s t-test.

    Article Snippet: ApoE levels in mouse sera were quantified using the mouse apoE ELISA PRO kit from Mabtech (Cincinnati, OH) as per the manufacturer’s directions.

    Techniques: Cell Culture, Flow Cytometry, Control, Cell Cycle Assay, Two Tailed Test

    ApoE agonist peptide COG133 inhibits cytokine secretion induced by immunogenic tumor cells, while anti-APOE blocking antibody enhances cytokine secretion in tumor cell/splenocyte reactions. (A) Naïve and vaccinated splenocyte production of IFNγ was markedly reduced when splenocytes were co-cultured with immunogenic (BET/JQ1 treated) B16 tumor cells in the presence of the apoE agonist COG133. (B) Naïve splenocyte production of IFNγ was significantly increased when co-cultured with immunogenic B16 tumor cells with anti-APOE antibody. (C) . COG133 was also inhibitory of IFNγ production when vaccinated splenocytes were used for co-culture with treated immunogenic cancer cells. It is of interest to note that the levels of IFNγ production is significantly greater when vaccinated splenocytes were used for this experiment. NS: naïve splenocytes, splenocytes were collected from naïve C57BL/6 mice. Treated B16: B16 cells were expose to Myc inhibitor (0.25µM BET and 0.25µM JQ1) for 4 days, to induce immunogenicity. VS: vaccinated splenocytes. Irradiated 10 4 WT B16 tumor cells and 100ug/ml anti-CTLA4 antibody were administered to C57BL/6 mice on day 0, and splenocytes were collected at day 7 after tumor cell inoculation. Data are representative of three independent experiments. Results are expressed as mean score ± SD. *p<0.05; **p<0.005; ***p<0.001, determined by unpaired two-tailed Student’s t-test.

    Journal: Frontiers in Immunology

    Article Title: Tumor Apolipoprotein E is a key checkpoint blocking anti-tumor immunity in mouse melanoma

    doi: 10.3389/fimmu.2022.991790

    Figure Lengend Snippet: ApoE agonist peptide COG133 inhibits cytokine secretion induced by immunogenic tumor cells, while anti-APOE blocking antibody enhances cytokine secretion in tumor cell/splenocyte reactions. (A) Naïve and vaccinated splenocyte production of IFNγ was markedly reduced when splenocytes were co-cultured with immunogenic (BET/JQ1 treated) B16 tumor cells in the presence of the apoE agonist COG133. (B) Naïve splenocyte production of IFNγ was significantly increased when co-cultured with immunogenic B16 tumor cells with anti-APOE antibody. (C) . COG133 was also inhibitory of IFNγ production when vaccinated splenocytes were used for co-culture with treated immunogenic cancer cells. It is of interest to note that the levels of IFNγ production is significantly greater when vaccinated splenocytes were used for this experiment. NS: naïve splenocytes, splenocytes were collected from naïve C57BL/6 mice. Treated B16: B16 cells were expose to Myc inhibitor (0.25µM BET and 0.25µM JQ1) for 4 days, to induce immunogenicity. VS: vaccinated splenocytes. Irradiated 10 4 WT B16 tumor cells and 100ug/ml anti-CTLA4 antibody were administered to C57BL/6 mice on day 0, and splenocytes were collected at day 7 after tumor cell inoculation. Data are representative of three independent experiments. Results are expressed as mean score ± SD. *p<0.05; **p<0.005; ***p<0.001, determined by unpaired two-tailed Student’s t-test.

    Article Snippet: ApoE levels in mouse sera were quantified using the mouse apoE ELISA PRO kit from Mabtech (Cincinnati, OH) as per the manufacturer’s directions.

    Techniques: Blocking Assay, Cell Culture, Co-Culture Assay, Immunopeptidomics, Irradiation, Two Tailed Test

    lrp8 is the most dominant receptor expressed on activated T cells and blocking lrp8 enhanced T-cell activation. (A) Expression of apoE receptors shows predominance of ldlr and lrp8 receptors on T cells, (B) lrp8, ldl and lrp1 receptors on dendritic cells, and (C) lrp1 receptors on macrophages as shown by quantitative real-time PCR (qPCR). Expression of ldlr and lrp8 was upregulated following T cell stimulation with CD3/CD28 beads. Expression of lrp8 was also upregulated following dendritic cell stimulation with TLR7/8. (D) The amount of IFNγ production from vaccinated splenocytes co-cultured with immunogenic WT B16 cells was quantified by ELISA assay. Results show that IFNγ production was significantly suppressed in the presence of the apoE agonist COG133, but suppression did not occur when splenocytes were harvested from lrp8 -/- mice. These findings suggest that T-cell function is at least partially inhibited by apoE through the lrp8 receptor pathway. Results are expressed as mean score ± SD. *p<0.05; **p<0.005; ***p<0.001, determined by unpaired two-tailed Student’s t-test.

    Journal: Frontiers in Immunology

    Article Title: Tumor Apolipoprotein E is a key checkpoint blocking anti-tumor immunity in mouse melanoma

    doi: 10.3389/fimmu.2022.991790

    Figure Lengend Snippet: lrp8 is the most dominant receptor expressed on activated T cells and blocking lrp8 enhanced T-cell activation. (A) Expression of apoE receptors shows predominance of ldlr and lrp8 receptors on T cells, (B) lrp8, ldl and lrp1 receptors on dendritic cells, and (C) lrp1 receptors on macrophages as shown by quantitative real-time PCR (qPCR). Expression of ldlr and lrp8 was upregulated following T cell stimulation with CD3/CD28 beads. Expression of lrp8 was also upregulated following dendritic cell stimulation with TLR7/8. (D) The amount of IFNγ production from vaccinated splenocytes co-cultured with immunogenic WT B16 cells was quantified by ELISA assay. Results show that IFNγ production was significantly suppressed in the presence of the apoE agonist COG133, but suppression did not occur when splenocytes were harvested from lrp8 -/- mice. These findings suggest that T-cell function is at least partially inhibited by apoE through the lrp8 receptor pathway. Results are expressed as mean score ± SD. *p<0.05; **p<0.005; ***p<0.001, determined by unpaired two-tailed Student’s t-test.

    Article Snippet: ApoE levels in mouse sera were quantified using the mouse apoE ELISA PRO kit from Mabtech (Cincinnati, OH) as per the manufacturer’s directions.

    Techniques: Blocking Assay, Activation Assay, Expressing, Real-time Polymerase Chain Reaction, Cell Stimulation, Cell Culture, Enzyme-linked Immunosorbent Assay, Cell Function Assay, Two Tailed Test

    Knock out of apoE in both B16 tumor cells and in mice enhances host immunity and attenuates tumorigenicity. (A) In vivo, 104 WT or apoE-/- B16 cells were injected into the right leg of WT (n=9), apoE-/- (n=9) or lrp8-/- mice (n=9). The average tumor growth in each group (n=6) is compared. Tumor growth was significantly slower when apoE-/- B16 cells were injected into apoE-/- or lrp8-/- mice versus the other groups (two-way ANOVA; P <0.0001). (B) The final tumor volume between treatment groups at the end point of the experiment (Day 20) was also compared using a one-way ANOVA followed by Tukey HSD pairwise multiple comparisons between treatment groups. Tumor volumes at the end point of the experiment were significantly different between treatment groups (one-way ANOVA; P <0.0001). *p<0.05; **p<0.01; ****p<0.0001.

    Journal: Frontiers in Immunology

    Article Title: Tumor Apolipoprotein E is a key checkpoint blocking anti-tumor immunity in mouse melanoma

    doi: 10.3389/fimmu.2022.991790

    Figure Lengend Snippet: Knock out of apoE in both B16 tumor cells and in mice enhances host immunity and attenuates tumorigenicity. (A) In vivo, 104 WT or apoE-/- B16 cells were injected into the right leg of WT (n=9), apoE-/- (n=9) or lrp8-/- mice (n=9). The average tumor growth in each group (n=6) is compared. Tumor growth was significantly slower when apoE-/- B16 cells were injected into apoE-/- or lrp8-/- mice versus the other groups (two-way ANOVA; P <0.0001). (B) The final tumor volume between treatment groups at the end point of the experiment (Day 20) was also compared using a one-way ANOVA followed by Tukey HSD pairwise multiple comparisons between treatment groups. Tumor volumes at the end point of the experiment were significantly different between treatment groups (one-way ANOVA; P <0.0001). *p<0.05; **p<0.01; ****p<0.0001.

    Article Snippet: ApoE levels in mouse sera were quantified using the mouse apoE ELISA PRO kit from Mabtech (Cincinnati, OH) as per the manufacturer’s directions.

    Techniques: Knock-Out, In Vivo, Injection

    Survival curve (A) Survival was significantly better (n=9) when apoE -/- B16 cells were injected into apoE -/- or lrp8 -/- mice versus the other groups. (B) The median survival time and the cumulative survival probability were calculated and compared using the Kaplan-Meier survival estimator followed by a log-rank test, and the hazard ratio (HR) was calculated using the Cox proportional-hazards regression model. The comparison between the groups is shown in the table.

    Journal: Frontiers in Immunology

    Article Title: Tumor Apolipoprotein E is a key checkpoint blocking anti-tumor immunity in mouse melanoma

    doi: 10.3389/fimmu.2022.991790

    Figure Lengend Snippet: Survival curve (A) Survival was significantly better (n=9) when apoE -/- B16 cells were injected into apoE -/- or lrp8 -/- mice versus the other groups. (B) The median survival time and the cumulative survival probability were calculated and compared using the Kaplan-Meier survival estimator followed by a log-rank test, and the hazard ratio (HR) was calculated using the Cox proportional-hazards regression model. The comparison between the groups is shown in the table.

    Article Snippet: ApoE levels in mouse sera were quantified using the mouse apoE ELISA PRO kit from Mabtech (Cincinnati, OH) as per the manufacturer’s directions.

    Techniques: Injection, Comparison

    The first three tumors that reached 15mm in each of the experimental groups were harvested and the immune cell infiltrate and immune pathway activation was analyzed with nanostring Pancancer immune profiling. (A) Immune cell type scores and (B) immune pathway (signature) scores show that immune cell infiltrates and immune pathway activation were greatest when apoE-/- cells were injected into apoE-/- mice. Dot line plots show the score trends of 12 immune cell lines and 29 immune pathways. Box plots show selective representative score comparisons. Results are expressed as mean score ±SD. *p<0.05, determined by unpaired two-tailed Student’s t-test. Wt/wt: wt B16 cells injected in wt mice; apoE-/-/apoE-/-: apoE-/- cells injected in apoE-/- mice; apoE-/-/lrp8-/-: apoE-/- cells injected in lrp8-/- mice; apoE-/-/wt: apoE-/- cells injected in wt mice; wt/apoE-/-: wt cells injected in apoE-/- mice; wt//lrp8-/-: wt cells injected in lrp8-/- mice.

    Journal: Frontiers in Immunology

    Article Title: Tumor Apolipoprotein E is a key checkpoint blocking anti-tumor immunity in mouse melanoma

    doi: 10.3389/fimmu.2022.991790

    Figure Lengend Snippet: The first three tumors that reached 15mm in each of the experimental groups were harvested and the immune cell infiltrate and immune pathway activation was analyzed with nanostring Pancancer immune profiling. (A) Immune cell type scores and (B) immune pathway (signature) scores show that immune cell infiltrates and immune pathway activation were greatest when apoE-/- cells were injected into apoE-/- mice. Dot line plots show the score trends of 12 immune cell lines and 29 immune pathways. Box plots show selective representative score comparisons. Results are expressed as mean score ±SD. *p<0.05, determined by unpaired two-tailed Student’s t-test. Wt/wt: wt B16 cells injected in wt mice; apoE-/-/apoE-/-: apoE-/- cells injected in apoE-/- mice; apoE-/-/lrp8-/-: apoE-/- cells injected in lrp8-/- mice; apoE-/-/wt: apoE-/- cells injected in wt mice; wt/apoE-/-: wt cells injected in apoE-/- mice; wt//lrp8-/-: wt cells injected in lrp8-/- mice.

    Article Snippet: ApoE levels in mouse sera were quantified using the mouse apoE ELISA PRO kit from Mabtech (Cincinnati, OH) as per the manufacturer’s directions.

    Techniques: Activation Assay, Injection, Two Tailed Test

    Nanostring PanCancer Immune Profiling analysis of RNAseq of activation markers for T cells and DCs that infiltrated into the tumors from the 6 different groups. (A) Activated T cell genes and (B) activated DC genes were all statistically significantly increased in the tumor from apoE-/-/apoE-/- group when compared with wt/wt control groups. The relative gene expression level was indicated on the y-axis and tumor groups are listed along the x-axis. Results are expressed as mean score ±SE. *p<0.05, determined by unpaired two-tailed Student’s t-test.

    Journal: Frontiers in Immunology

    Article Title: Tumor Apolipoprotein E is a key checkpoint blocking anti-tumor immunity in mouse melanoma

    doi: 10.3389/fimmu.2022.991790

    Figure Lengend Snippet: Nanostring PanCancer Immune Profiling analysis of RNAseq of activation markers for T cells and DCs that infiltrated into the tumors from the 6 different groups. (A) Activated T cell genes and (B) activated DC genes were all statistically significantly increased in the tumor from apoE-/-/apoE-/- group when compared with wt/wt control groups. The relative gene expression level was indicated on the y-axis and tumor groups are listed along the x-axis. Results are expressed as mean score ±SE. *p<0.05, determined by unpaired two-tailed Student’s t-test.

    Article Snippet: ApoE levels in mouse sera were quantified using the mouse apoE ELISA PRO kit from Mabtech (Cincinnati, OH) as per the manufacturer’s directions.

    Techniques: Activation Assay, Control, Gene Expression, Two Tailed Test

    To validate nanostring results, both CD45 and CD3 expression were examined with IHC staining in the tumors from WT or apoE-/- mice following injection with WT or apoE-/- tumor cells. Representative images of CD45 (A) and CD3 (C) staining visualized with DAB (brown) and counterstained with hematoxylin (blue, nuclei). (B, D) Optical density (mean gray value) obtained by color deconvolution analysis. Optical density graph bars represent the mean ± SD (n = 30 images). ***p<0.001, determined by unpaired two-tailed Student’s t-test. Wt/wt: wt B16 cells injected in wt mice; apoE-/- /apoE-/-: apoE-/- cells injected in apoE-/- mice.

    Journal: Frontiers in Immunology

    Article Title: Tumor Apolipoprotein E is a key checkpoint blocking anti-tumor immunity in mouse melanoma

    doi: 10.3389/fimmu.2022.991790

    Figure Lengend Snippet: To validate nanostring results, both CD45 and CD3 expression were examined with IHC staining in the tumors from WT or apoE-/- mice following injection with WT or apoE-/- tumor cells. Representative images of CD45 (A) and CD3 (C) staining visualized with DAB (brown) and counterstained with hematoxylin (blue, nuclei). (B, D) Optical density (mean gray value) obtained by color deconvolution analysis. Optical density graph bars represent the mean ± SD (n = 30 images). ***p<0.001, determined by unpaired two-tailed Student’s t-test. Wt/wt: wt B16 cells injected in wt mice; apoE-/- /apoE-/-: apoE-/- cells injected in apoE-/- mice.

    Article Snippet: ApoE levels in mouse sera were quantified using the mouse apoE ELISA PRO kit from Mabtech (Cincinnati, OH) as per the manufacturer’s directions.

    Techniques: Expressing, Immunohistochemistry, Injection, Staining, Two Tailed Test

    ApoE knock out in B16 tumor cells induces potent immunogenicity. Wild type and apoE -/- mice (A) or wild type and lrp8 -/- mice (B) , were inoculated with either WT B16 or apoE -/- cells, with anti-CTLA4 antibody on day 0. Splenocytes were harvested on day 7 and co-cultured with either WT B16 or apoE -/- B16 cells for 48hr, following which IFNγ levels in media were compared with ELISA assay. Results show that IFNγ production is highest for all groups when apoE -/- cells are used. These findings re-iterate the potent inhibitory effect of apoE on immune cell activation in the cancer environment. Results are expressed as mean score ± SD. *p<0.05; **p<0.005; ***p<0.001, determined by unpaired two-tailed Student’s t-test.

    Journal: Frontiers in Immunology

    Article Title: Tumor Apolipoprotein E is a key checkpoint blocking anti-tumor immunity in mouse melanoma

    doi: 10.3389/fimmu.2022.991790

    Figure Lengend Snippet: ApoE knock out in B16 tumor cells induces potent immunogenicity. Wild type and apoE -/- mice (A) or wild type and lrp8 -/- mice (B) , were inoculated with either WT B16 or apoE -/- cells, with anti-CTLA4 antibody on day 0. Splenocytes were harvested on day 7 and co-cultured with either WT B16 or apoE -/- B16 cells for 48hr, following which IFNγ levels in media were compared with ELISA assay. Results show that IFNγ production is highest for all groups when apoE -/- cells are used. These findings re-iterate the potent inhibitory effect of apoE on immune cell activation in the cancer environment. Results are expressed as mean score ± SD. *p<0.05; **p<0.005; ***p<0.001, determined by unpaired two-tailed Student’s t-test.

    Article Snippet: ApoE levels in mouse sera were quantified using the mouse apoE ELISA PRO kit from Mabtech (Cincinnati, OH) as per the manufacturer’s directions.

    Techniques: Knock-Out, Immunopeptidomics, Cell Culture, Enzyme-linked Immunosorbent Assay, Activation Assay, Two Tailed Test

    ApoE RNA-seq expression is abundant in cutaneous melanoma but is not associated with PD-L1 or PD1. Scatterplots showing mRNA expression correlation of APOE (x-axis) with PD-L1, PD1 and APOC1 from the TCGA melanoma datasets based on their RNA-seq gene expression values (measured by RSEM algorithm). APOE expression did not correlate with PD-L1 or PD1 but did positively correlate with APOC1 expression which was used as a control gene. The correlation was evaluated by the Spearman correlation coefficient with a cut-off value of 0.5 and P-value used a cut-off value of 0.05.

    Journal: Frontiers in Immunology

    Article Title: Tumor Apolipoprotein E is a key checkpoint blocking anti-tumor immunity in mouse melanoma

    doi: 10.3389/fimmu.2022.991790

    Figure Lengend Snippet: ApoE RNA-seq expression is abundant in cutaneous melanoma but is not associated with PD-L1 or PD1. Scatterplots showing mRNA expression correlation of APOE (x-axis) with PD-L1, PD1 and APOC1 from the TCGA melanoma datasets based on their RNA-seq gene expression values (measured by RSEM algorithm). APOE expression did not correlate with PD-L1 or PD1 but did positively correlate with APOC1 expression which was used as a control gene. The correlation was evaluated by the Spearman correlation coefficient with a cut-off value of 0.5 and P-value used a cut-off value of 0.05.

    Article Snippet: ApoE levels in mouse sera were quantified using the mouse apoE ELISA PRO kit from Mabtech (Cincinnati, OH) as per the manufacturer’s directions.

    Techniques: RNA Sequencing, Expressing, Gene Expression, Control

    Scatterplots show the tumor purity-corrected partial Spearman’s rho value and the correlation between gene expression with infiltration of six immune cell estimates. Top row is APOE expression while the bottom row depicts PD-L1. PD-L1 correlated with CD8 T cell and neutrophil infiltrates, while APOE does not correlate with immune cell infiltrates. The correlation was evaluated by the Spearman correlation coefficient with a cut-off value of 0.5 and P-value used a cut-off value of 0.05.

    Journal: Frontiers in Immunology

    Article Title: Tumor Apolipoprotein E is a key checkpoint blocking anti-tumor immunity in mouse melanoma

    doi: 10.3389/fimmu.2022.991790

    Figure Lengend Snippet: Scatterplots show the tumor purity-corrected partial Spearman’s rho value and the correlation between gene expression with infiltration of six immune cell estimates. Top row is APOE expression while the bottom row depicts PD-L1. PD-L1 correlated with CD8 T cell and neutrophil infiltrates, while APOE does not correlate with immune cell infiltrates. The correlation was evaluated by the Spearman correlation coefficient with a cut-off value of 0.5 and P-value used a cut-off value of 0.05.

    Article Snippet: ApoE levels in mouse sera were quantified using the mouse apoE ELISA PRO kit from Mabtech (Cincinnati, OH) as per the manufacturer’s directions.

    Techniques: Gene Expression, Expressing

    Cumulative survival of patients associated with bifurcate gene expression at 30%. TCGA database includes primary and metastasis samples (n=462). APOE expression did not associate with survival, while PD-L1 and PD1 was associated with survival at this level of analysis. The correlation was evaluated by the Spearman correlation coefficient with a cut-off value of 0.5 and P-value used a cut-off value of 0.05.

    Journal: Frontiers in Immunology

    Article Title: Tumor Apolipoprotein E is a key checkpoint blocking anti-tumor immunity in mouse melanoma

    doi: 10.3389/fimmu.2022.991790

    Figure Lengend Snippet: Cumulative survival of patients associated with bifurcate gene expression at 30%. TCGA database includes primary and metastasis samples (n=462). APOE expression did not associate with survival, while PD-L1 and PD1 was associated with survival at this level of analysis. The correlation was evaluated by the Spearman correlation coefficient with a cut-off value of 0.5 and P-value used a cut-off value of 0.05.

    Article Snippet: ApoE levels in mouse sera were quantified using the mouse apoE ELISA PRO kit from Mabtech (Cincinnati, OH) as per the manufacturer’s directions.

    Techniques: Gene Expression, Expressing