mouse anti cd276 Search Results


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Bio X Cell anti mouse cd276
<t>CD276</t> + macrophages are abundant in tumor tissues and correlated with T-cell immunity in PNEN TME. A, Representative IHC images of CD68 and CD276 in tumor and nontumor tissues (scale bar: 200 mm). B, Representative mIHC images of CD68 and CD276 in tumor and nontumor tissues (scale bar: 20 mm). The percentage of CD276 + macrophages was higher in tumor tissues (15 pairs of tumor and nontumor tissues). C, Representative mIHC images of CD68, CD276, and CD3. The negative correlation between the number of CD276 + CD68 + cells and CD3 + T cells in the 20 field from 22 PNEN tissue samples (scale bar: 20 μm). D, Representative IHC images of CD68, CD276, CD3, and CD8 (scale bar: 100 μm). E, CD276 + macrophage infiltration in tumors of PNEN with liver metastasis (LM) was higher than that in PNEN without liver metastasis. F, Data of EGA database with 84 patients with PNEN showed that high CD276 expression was associated with the lymph node metastasis, high histopathologic grade, TNM stage, metastasis, and poor survival. Box plots show the median (central line) and cover the interquartile interval. ***, P < 0.001.
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CD276 + macrophages are abundant in tumor tissues and correlated with T-cell immunity in PNEN TME. A, Representative IHC images of CD68 and CD276 in tumor and nontumor tissues (scale bar: 200 mm). B, Representative mIHC images of CD68 and CD276 in tumor and nontumor tissues (scale bar: 20 mm). The percentage of CD276 + macrophages was higher in tumor tissues (15 pairs of tumor and nontumor tissues). C, Representative mIHC images of CD68, CD276, and CD3. The negative correlation between the number of CD276 + CD68 + cells and CD3 + T cells in the 20 field from 22 PNEN tissue samples (scale bar: 20 μm). D, Representative IHC images of CD68, CD276, CD3, and CD8 (scale bar: 100 μm). E, CD276 + macrophage infiltration in tumors of PNEN with liver metastasis (LM) was higher than that in PNEN without liver metastasis. F, Data of EGA database with 84 patients with PNEN showed that high CD276 expression was associated with the lymph node metastasis, high histopathologic grade, TNM stage, metastasis, and poor survival. Box plots show the median (central line) and cover the interquartile interval. ***, P < 0.001.

Journal: Cancer Immunology Research

Article Title: Small Extracellular Vesicle piR-hsa-30937 Derived from Pancreatic Neuroendocrine Neoplasms Upregulates CD276 in Macrophages to Promote Immune Evasion

doi: 10.1158/2326-6066.CIR-23-0825

Figure Lengend Snippet: CD276 + macrophages are abundant in tumor tissues and correlated with T-cell immunity in PNEN TME. A, Representative IHC images of CD68 and CD276 in tumor and nontumor tissues (scale bar: 200 mm). B, Representative mIHC images of CD68 and CD276 in tumor and nontumor tissues (scale bar: 20 mm). The percentage of CD276 + macrophages was higher in tumor tissues (15 pairs of tumor and nontumor tissues). C, Representative mIHC images of CD68, CD276, and CD3. The negative correlation between the number of CD276 + CD68 + cells and CD3 + T cells in the 20 field from 22 PNEN tissue samples (scale bar: 20 μm). D, Representative IHC images of CD68, CD276, CD3, and CD8 (scale bar: 100 μm). E, CD276 + macrophage infiltration in tumors of PNEN with liver metastasis (LM) was higher than that in PNEN without liver metastasis. F, Data of EGA database with 84 patients with PNEN showed that high CD276 expression was associated with the lymph node metastasis, high histopathologic grade, TNM stage, metastasis, and poor survival. Box plots show the median (central line) and cover the interquartile interval. ***, P < 0.001.

Article Snippet: Anti-mouse CD276 (BioXcell) or the isotype control IgG was administrated intraperitoneally at 100 μg per mouse on days 9, 12, 15, and 18.

Techniques: Expressing

Coculture with PNEN cells drive CD276 expression in macrophages to inhibit T-cell immunity. A and B, THP-1 macrophages and hMDMs were cocultured with PNEN cells or HPNE cells for 48 hours and then flow cytometry detected CD276 expression and the mean fluorescence intensity (MFI) was analyzed. C, After coculture with HPNE or QGP-1, macrophages were cocultured with CFSE-labeled human PBLs with or without anti-CD276 neutralizing antibodies. Flow cytometry detected CD3 + T-cell proliferation and IFNγ production and data were statistical analyzed. Data are shown as mean ± SD. Each experiment contained three independent biological replicates. ***, P < 0.001.

Journal: Cancer Immunology Research

Article Title: Small Extracellular Vesicle piR-hsa-30937 Derived from Pancreatic Neuroendocrine Neoplasms Upregulates CD276 in Macrophages to Promote Immune Evasion

doi: 10.1158/2326-6066.CIR-23-0825

Figure Lengend Snippet: Coculture with PNEN cells drive CD276 expression in macrophages to inhibit T-cell immunity. A and B, THP-1 macrophages and hMDMs were cocultured with PNEN cells or HPNE cells for 48 hours and then flow cytometry detected CD276 expression and the mean fluorescence intensity (MFI) was analyzed. C, After coculture with HPNE or QGP-1, macrophages were cocultured with CFSE-labeled human PBLs with or without anti-CD276 neutralizing antibodies. Flow cytometry detected CD3 + T-cell proliferation and IFNγ production and data were statistical analyzed. Data are shown as mean ± SD. Each experiment contained three independent biological replicates. ***, P < 0.001.

Article Snippet: Anti-mouse CD276 (BioXcell) or the isotype control IgG was administrated intraperitoneally at 100 μg per mouse on days 9, 12, 15, and 18.

Techniques: Expressing, Flow Cytometry, Fluorescence, Labeling

PNEN cell–derived sEVs drive CD276 expression in THP-1 macrophages to inhibit T-cell immunity. A, Transmission electron micrograph and nanoparticle tracking analysis of sEVs derived from HPNE, QGP-1, and BON-1 (scale bar: 100 nm). B, HSP70, CD63, TSG101, and calnexin were examined for cells and sEVs by Western blot analysis. C, Representative fluorescent images of the internalization of PKH26-labeled sEVs by macrophages (scale bar: 50 μm). D, THP-1 macrophages were incubated with 10 μg/ml sEVs derived from HPNE or PNEN cells for 48 hours and CD276 expression was detected by flow cytometry. E, CFSE-labeled PBLs were cocultured with THP-1 macrophages treated by 10 mg/mL sEVs derived from HPNE or PNEN cells with or without anti-CD276 neutralizing antibodies. Flow cytometry detected CD3 + and CD8 + T-cell proliferation and IFNγ production. Data are shown as mean ± SD. Each experiment contained three independent biological replicates. ***, P < 0.001.

Journal: Cancer Immunology Research

Article Title: Small Extracellular Vesicle piR-hsa-30937 Derived from Pancreatic Neuroendocrine Neoplasms Upregulates CD276 in Macrophages to Promote Immune Evasion

doi: 10.1158/2326-6066.CIR-23-0825

Figure Lengend Snippet: PNEN cell–derived sEVs drive CD276 expression in THP-1 macrophages to inhibit T-cell immunity. A, Transmission electron micrograph and nanoparticle tracking analysis of sEVs derived from HPNE, QGP-1, and BON-1 (scale bar: 100 nm). B, HSP70, CD63, TSG101, and calnexin were examined for cells and sEVs by Western blot analysis. C, Representative fluorescent images of the internalization of PKH26-labeled sEVs by macrophages (scale bar: 50 μm). D, THP-1 macrophages were incubated with 10 μg/ml sEVs derived from HPNE or PNEN cells for 48 hours and CD276 expression was detected by flow cytometry. E, CFSE-labeled PBLs were cocultured with THP-1 macrophages treated by 10 mg/mL sEVs derived from HPNE or PNEN cells with or without anti-CD276 neutralizing antibodies. Flow cytometry detected CD3 + and CD8 + T-cell proliferation and IFNγ production. Data are shown as mean ± SD. Each experiment contained three independent biological replicates. ***, P < 0.001.

Article Snippet: Anti-mouse CD276 (BioXcell) or the isotype control IgG was administrated intraperitoneally at 100 μg per mouse on days 9, 12, 15, and 18.

Techniques: Derivative Assay, Expressing, Transmission Assay, Western Blot, Labeling, Incubation, Flow Cytometry

PNEN cell-derived sEV piR-hsa-30937 drives CD276 expression in macrophages to inhibit T-cell activity. A, Macrophages were incubated with sEVs derived from shpiR-hsa-30937 or shNC PNEN cells, and CD276 expression was detected by flow cytometry. B, Macrophages were transfected with piR-NC or piR-hsa-30937, and CD276 expression was detected by flow cytometry. C, Macrophages were transfected with shNC or shPTEN, and CD276 expression was detected by flow cytometry. D, CFSE-labeled PBLs were cocultured with macrophages treated by shpiR-hsa-30937 or shNC PNEN cell-derived sEVs. Flow cytometry detected CD3 + T-cell proliferation and IFNγ production. E, CFSE-labeled PBLs were cocultured with macrophages transfected with piR-NC or piR-hsa-30937 with or without anti-CD276 neutralizing antibodies. Flow cytometry detected CD3 + T-cell proliferation and IFNγ production. Data are shown as mean SD. Each experiment contained three independent biological replicates. **, P < 0.01; ***, P < 0.001.

Journal: Cancer Immunology Research

Article Title: Small Extracellular Vesicle piR-hsa-30937 Derived from Pancreatic Neuroendocrine Neoplasms Upregulates CD276 in Macrophages to Promote Immune Evasion

doi: 10.1158/2326-6066.CIR-23-0825

Figure Lengend Snippet: PNEN cell-derived sEV piR-hsa-30937 drives CD276 expression in macrophages to inhibit T-cell activity. A, Macrophages were incubated with sEVs derived from shpiR-hsa-30937 or shNC PNEN cells, and CD276 expression was detected by flow cytometry. B, Macrophages were transfected with piR-NC or piR-hsa-30937, and CD276 expression was detected by flow cytometry. C, Macrophages were transfected with shNC or shPTEN, and CD276 expression was detected by flow cytometry. D, CFSE-labeled PBLs were cocultured with macrophages treated by shpiR-hsa-30937 or shNC PNEN cell-derived sEVs. Flow cytometry detected CD3 + T-cell proliferation and IFNγ production. E, CFSE-labeled PBLs were cocultured with macrophages transfected with piR-NC or piR-hsa-30937 with or without anti-CD276 neutralizing antibodies. Flow cytometry detected CD3 + T-cell proliferation and IFNγ production. Data are shown as mean SD. Each experiment contained three independent biological replicates. **, P < 0.01; ***, P < 0.001.

Article Snippet: Anti-mouse CD276 (BioXcell) or the isotype control IgG was administrated intraperitoneally at 100 μg per mouse on days 9, 12, 15, and 18.

Techniques: Derivative Assay, Expressing, Activity Assay, Incubation, Flow Cytometry, Transfection, Labeling

NEN cell–derived sEV piR-hsa-30937 drives CD276 expression in macrophages by targeting PTEN to activate the AKT signaling pathway. A, Potential binding sites between piR-hsa-30937 and PTEN 3′ UTR. B, Effects of piR-hsa-30937 or piR-NC on the luciferase activity of the reporters containing the WT or MUT PTEN 3′ UTR were measured by luciferase reporter gene activity. Luciferase activity was normalized to renilla luciferase activity. C, Macrophages were treated by 10 mg/mL shpiR hsa-30937 or shNC PNEN cell-derived sEVs. Macrophages were transfected with piR-hsa-30937 or shPTEN and corresponding controls. The expression of CD276, PTEN, and p-AKT of macrophages were examined by Western blot analysis. D, Macrophages were treated by PNEN cell–derived sEVs with or without MK-2206 (10 μmol/L). Flow cytometry detected CD276 expression of macrophages. Data are shown as mean SD. Each experiment contained three independent biological replicates. ***, P < 0.001.

Journal: Cancer Immunology Research

Article Title: Small Extracellular Vesicle piR-hsa-30937 Derived from Pancreatic Neuroendocrine Neoplasms Upregulates CD276 in Macrophages to Promote Immune Evasion

doi: 10.1158/2326-6066.CIR-23-0825

Figure Lengend Snippet: NEN cell–derived sEV piR-hsa-30937 drives CD276 expression in macrophages by targeting PTEN to activate the AKT signaling pathway. A, Potential binding sites between piR-hsa-30937 and PTEN 3′ UTR. B, Effects of piR-hsa-30937 or piR-NC on the luciferase activity of the reporters containing the WT or MUT PTEN 3′ UTR were measured by luciferase reporter gene activity. Luciferase activity was normalized to renilla luciferase activity. C, Macrophages were treated by 10 mg/mL shpiR hsa-30937 or shNC PNEN cell-derived sEVs. Macrophages were transfected with piR-hsa-30937 or shPTEN and corresponding controls. The expression of CD276, PTEN, and p-AKT of macrophages were examined by Western blot analysis. D, Macrophages were treated by PNEN cell–derived sEVs with or without MK-2206 (10 μmol/L). Flow cytometry detected CD276 expression of macrophages. Data are shown as mean SD. Each experiment contained three independent biological replicates. ***, P < 0.001.

Article Snippet: Anti-mouse CD276 (BioXcell) or the isotype control IgG was administrated intraperitoneally at 100 μg per mouse on days 9, 12, 15, and 18.

Techniques: Derivative Assay, Expressing, Binding Assay, Luciferase, Activity Assay, Transfection, Western Blot, Flow Cytometry

piR-hsa-30937 knockdown and CD276 blockade enhance T-cell immunity to inhibit PNEN growth and metastasis in vivo . A, Tumor volumes and weights. B, Representative mIHC images of F4/80, CD276, and CD3 (scale bar: 20 μm). C, Representative images of Ki67 staining and the lung metastasis and liver metastasis by hematoxylin and eosin staining (scale bar: 100 μm). Data are shown as mean ±SD. ***, P < 0.001.

Journal: Cancer Immunology Research

Article Title: Small Extracellular Vesicle piR-hsa-30937 Derived from Pancreatic Neuroendocrine Neoplasms Upregulates CD276 in Macrophages to Promote Immune Evasion

doi: 10.1158/2326-6066.CIR-23-0825

Figure Lengend Snippet: piR-hsa-30937 knockdown and CD276 blockade enhance T-cell immunity to inhibit PNEN growth and metastasis in vivo . A, Tumor volumes and weights. B, Representative mIHC images of F4/80, CD276, and CD3 (scale bar: 20 μm). C, Representative images of Ki67 staining and the lung metastasis and liver metastasis by hematoxylin and eosin staining (scale bar: 100 μm). Data are shown as mean ±SD. ***, P < 0.001.

Article Snippet: Anti-mouse CD276 (BioXcell) or the isotype control IgG was administrated intraperitoneally at 100 μg per mouse on days 9, 12, 15, and 18.

Techniques: Knockdown, In Vivo, Staining