mouse b7h3 (Bio X Cell)

Bio X Cell is a verified supplier

Bio X Cell manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Bio X Cell mouse b7h3

Clinical significance of circulating MDSCs and association with regulatory T cells and <t>B7H3</t> + cells. Regression and correlation analyses were performed for MDSC abundance in peripheral blood and its relationship to lung function. The correlations between lung function (DLO, % predicted) and the frequencies of MDSCs (A) , G-MDSCs (B) , and M-MDSCs (C) are shown. N = 62. p < 0.05 in panels A–C. (D) The frequency of M-MDSCs in samples from the IPF patients without treatment was plotted for the correlation analysis. N = 17. p < 0.05. (E) The IPF patient samples were separated into untreated and treated (with pirfenidone or nintedanib) groups, and the M-MDSC frequency was compared between these two groups. N = 22 in untreated; N = 44 in treated IPF group. *p < 0.05. (F) Circulating CD4 + CD25 + regulatory T cells were analyzed in whole blood showing a positive correlation between the frequency of whole blood total MDSC and regulatory T cells. N = 31. p < 0.001. CD4 + CD25 + T-cell correlation between G-MDSC (G) and M-MDSC (H) is shown. N = 33. p < 0.001. The frequency of B7H3 + cells was analyzed, and the correlation with MDSC (I) , G-MDSC (J) , and M-MDSC (K) is shown. N = 42 in panels I and J, and 40 in panel (K) p < 0.05 in panel (I) , p < 0.01 in panel (J) , and p < 0.0001 in panel (K) MDSCs, myeloid-derived suppressor cells; DLCO, diffusing capacity of the lungs for carbon monoxide; G-MDSCs, granulocytic myeloid-derived suppressor cells; M-MDSCs, monocytic myeloid-derived suppressor cells.

Mouse B7h3, supplied by Bio X Cell, used in various techniques. Bioz Stars score: 94/100, based on 22 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sequencing-based+spatial+transcriptomics+data/InVivoMAb+anti-mouse+CD276/pmc09420866-48-12-14
Average 94 stars, based on 22 article reviews

mouse b7h3 - by Bioz Stars, 2026-09

94/100 stars

Images

1) Product Images from "B7H3-dependent myeloid-derived suppressor cell recruitment and activation in pulmonary fibrosis"

Article Title: B7H3-dependent myeloid-derived suppressor cell recruitment and activation in pulmonary fibrosis

Journal: Frontiers in Immunology

doi: 10.3389/fimmu.2022.901349

Clinical significance of circulating MDSCs and association with regulatory T cells and B7H3 + cells. Regression and correlation analyses were performed for MDSC abundance in peripheral blood and its relationship to lung function. The correlations between lung function (DLO, % predicted) and the frequencies of MDSCs (A) , G-MDSCs (B) , and M-MDSCs (C) are shown. N = 62. p < 0.05 in panels A–C. (D) The frequency of M-MDSCs in samples from the IPF patients without treatment was plotted for the correlation analysis. N = 17. p < 0.05. (E) The IPF patient samples were separated into untreated and treated (with pirfenidone or nintedanib) groups, and the M-MDSC frequency was compared between these two groups. N = 22 in untreated; N = 44 in treated IPF group. *p < 0.05. (F) Circulating CD4 + CD25 + regulatory T cells were analyzed in whole blood showing a positive correlation between the frequency of whole blood total MDSC and regulatory T cells. N = 31. p < 0.001. CD4 + CD25 + T-cell correlation between G-MDSC (G) and M-MDSC (H) is shown. N = 33. p < 0.001. The frequency of B7H3 + cells was analyzed, and the correlation with MDSC (I) , G-MDSC (J) , and M-MDSC (K) is shown. N = 42 in panels I and J, and 40 in panel (K) p < 0.05 in panel (I) , p < 0.01 in panel (J) , and p < 0.0001 in panel (K) MDSCs, myeloid-derived suppressor cells; DLCO, diffusing capacity of the lungs for carbon monoxide; G-MDSCs, granulocytic myeloid-derived suppressor cells; M-MDSCs, monocytic myeloid-derived suppressor cells.

Figure Legend Snippet: Clinical significance of circulating MDSCs and association with regulatory T cells and B7H3 + cells. Regression and correlation analyses were performed for MDSC abundance in peripheral blood and its relationship to lung function. The correlations between lung function (DLO, % predicted) and the frequencies of MDSCs (A) , G-MDSCs (B) , and M-MDSCs (C) are shown. N = 62. p < 0.05 in panels A–C. (D) The frequency of M-MDSCs in samples from the IPF patients without treatment was plotted for the correlation analysis. N = 17. p < 0.05. (E) The IPF patient samples were separated into untreated and treated (with pirfenidone or nintedanib) groups, and the M-MDSC frequency was compared between these two groups. N = 22 in untreated; N = 44 in treated IPF group. *p < 0.05. (F) Circulating CD4 + CD25 + regulatory T cells were analyzed in whole blood showing a positive correlation between the frequency of whole blood total MDSC and regulatory T cells. N = 31. p < 0.001. CD4 + CD25 + T-cell correlation between G-MDSC (G) and M-MDSC (H) is shown. N = 33. p < 0.001. The frequency of B7H3 + cells was analyzed, and the correlation with MDSC (I) , G-MDSC (J) , and M-MDSC (K) is shown. N = 42 in panels I and J, and 40 in panel (K) p < 0.05 in panel (I) , p < 0.01 in panel (J) , and p < 0.0001 in panel (K) MDSCs, myeloid-derived suppressor cells; DLCO, diffusing capacity of the lungs for carbon monoxide; G-MDSCs, granulocytic myeloid-derived suppressor cells; M-MDSCs, monocytic myeloid-derived suppressor cells.

Techniques Used: Derivative Assay

B7H3-activated MDSC promoted fibroblast activation/myofibroblast differentiation and suppressed T-cell proliferation. BM-derived MDSCs were treated with sB7H3 (4 µg/ml) or SCF (0.1 µg/ml) in presence of GM-CSF (0.01 µg/ml) for 3 days followed by flow cytometric cell sorting. Sorted G-MDSCs or M-MDSCs were co-cultured with primary isolated MLF in 24-well transwell plates (ratio of MDSC : MLF = 2:1). After 48 h of co-culture, RNA from MLF was isolated and analyzed by qPCR for type I collagen (Col1a2) (A) , α-SMA (Acta2) (B) , and TGFβ1 (Tgfb1) expression (C) . Cellular RNA from sorted G-MDSCs and M-MDSCs was also extracted and similarly analyzed for expression of TGFβ1 (Tgfb1) (D) . The 18S RNA was used as internal control for normalization. The data were expressed as fold change relative to the respective control. (E) B7H3 blocking antibody (Ab) was injected intravenously into mice after BLM treatment. The lung single-cell suspensions were obtained 7 days after BLM treatment for flow cytometry analysis of MDSCs. Representative plots (pre-gated by CD45 + CD11b + cells) are shown on the left panel and the quantitative analysis of percentages and absolute cell numbers on the middle and right panels, respectively. (F) Total lung cell numbers were counted using a hemocytometer. (G) Lung tissue RNA was analyzed by qPCR for Tnfa , Col1a1 , and Acta2 on day 7 after BLM treatment. (H) BM-derived CD11b + Gr1 + MDSCs with (+) or without (−) sB7H3 activation were co-cultured with CFSE pre-labeled splenocytes in media only (Naïve T cell) or in stimulation medium containing CD3/28 Dynabeads+rmIL2 (Activated T-cell) for 3 days. CD4 + or CD8 + T-cell proliferation was assessed by counting CFSE + cells with either T-cell marker using flow cytometry. (I) Fresh BM cells were treated with sB7H3 for 72 h and analyzed for CD84 and MDSC markers. The data were shown as the percentage (left) or the absolute numbers per million BM cells (right) of G-MDSC or M-MDSC in the CD84-expressing CD11b + BM population. Mean ± SD is shown for all. N = 3–8. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001. MDSC, myeloid-derived suppressor cell; BM, bone marrow; sB7H3, soluble B7H3; SCF, stem cell factor; GM-CSF, granulocyte-macrophage colony-stimulating factor; MLF, mouse lung fibroblast; BLM, bleomycin; CFSE, carboxyfluorescein succinimidyl ester.

Figure Legend Snippet: B7H3-activated MDSC promoted fibroblast activation/myofibroblast differentiation and suppressed T-cell proliferation. BM-derived MDSCs were treated with sB7H3 (4 µg/ml) or SCF (0.1 µg/ml) in presence of GM-CSF (0.01 µg/ml) for 3 days followed by flow cytometric cell sorting. Sorted G-MDSCs or M-MDSCs were co-cultured with primary isolated MLF in 24-well transwell plates (ratio of MDSC : MLF = 2:1). After 48 h of co-culture, RNA from MLF was isolated and analyzed by qPCR for type I collagen (Col1a2) (A) , α-SMA (Acta2) (B) , and TGFβ1 (Tgfb1) expression (C) . Cellular RNA from sorted G-MDSCs and M-MDSCs was also extracted and similarly analyzed for expression of TGFβ1 (Tgfb1) (D) . The 18S RNA was used as internal control for normalization. The data were expressed as fold change relative to the respective control. (E) B7H3 blocking antibody (Ab) was injected intravenously into mice after BLM treatment. The lung single-cell suspensions were obtained 7 days after BLM treatment for flow cytometry analysis of MDSCs. Representative plots (pre-gated by CD45 + CD11b + cells) are shown on the left panel and the quantitative analysis of percentages and absolute cell numbers on the middle and right panels, respectively. (F) Total lung cell numbers were counted using a hemocytometer. (G) Lung tissue RNA was analyzed by qPCR for Tnfa , Col1a1 , and Acta2 on day 7 after BLM treatment. (H) BM-derived CD11b + Gr1 + MDSCs with (+) or without (−) sB7H3 activation were co-cultured with CFSE pre-labeled splenocytes in media only (Naïve T cell) or in stimulation medium containing CD3/28 Dynabeads+rmIL2 (Activated T-cell) for 3 days. CD4 + or CD8 + T-cell proliferation was assessed by counting CFSE + cells with either T-cell marker using flow cytometry. (I) Fresh BM cells were treated with sB7H3 for 72 h and analyzed for CD84 and MDSC markers. The data were shown as the percentage (left) or the absolute numbers per million BM cells (right) of G-MDSC or M-MDSC in the CD84-expressing CD11b + BM population. Mean ± SD is shown for all. N = 3–8. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001. MDSC, myeloid-derived suppressor cell; BM, bone marrow; sB7H3, soluble B7H3; SCF, stem cell factor; GM-CSF, granulocyte-macrophage colony-stimulating factor; MLF, mouse lung fibroblast; BLM, bleomycin; CFSE, carboxyfluorescein succinimidyl ester.

Techniques Used: Activation Assay, Derivative Assay, FACS, Cell Culture, Isolation, Co-Culture Assay, Expressing, Control, Blocking Assay, Injection, Flow Cytometry, Labeling, Marker

Lung scRNA-seq analysis identified B7H3-expressing cell clusters in human and mouse lung fibrosis. (A) Uniform manifold approximation and projection (UMAP) plots for all lung cells from IPF and control subjects were obtained from the IPF Cell Atlas online database ( CD276 expression was distributed in three distinct cell clusters shown in the top row). Diffusion map implementation labeled by cell type or disease status is shown in the middle row or the bottom row, respectively. (B) Level of CD276 in the lung cell clusters in IPF vs . control subjects. (C) Distribution of the expression signals for the indicated genes within the stromal cell cluster. (D) UMAP plots ( fibroXplorer.com ) of mouse lung fibroblasts identified as Dpt+ universal fibroblasts from BLM-treated lungs. Gene expression level for each gene is shown in the fibroblast sub-clusters. Lung fibroblast sub-clusters are color-coded (see left panel). (E) Pre-labeled MDSCs isolated from naïve BM were placed in the upper inserts. Cell-free CMs collected from untreated (control CM) or TGFβ-treated MLF (TGFβ-CM) cultures were incubated with B7H3 blocking antibody (Ab) or control IgG prior to placing in the lower chambers. The fluorescence intensity of the lower chamber was measured at 18 h of incubation. The data are presented as the percentages of TGFβ CMs over their respective control CMs. Mean ± SD are shown. N = 8/group. ****p < 0.0001. scRNA-seq, single-cell RNA sequencing; IPF, idiopathic pulmonary fibrosis; BLM, bleomycin; CMs, conditioned media; MLF, mouse lung fibroblast.

Figure Legend Snippet: Lung scRNA-seq analysis identified B7H3-expressing cell clusters in human and mouse lung fibrosis. (A) Uniform manifold approximation and projection (UMAP) plots for all lung cells from IPF and control subjects were obtained from the IPF Cell Atlas online database ( CD276 expression was distributed in three distinct cell clusters shown in the top row). Diffusion map implementation labeled by cell type or disease status is shown in the middle row or the bottom row, respectively. (B) Level of CD276 in the lung cell clusters in IPF vs . control subjects. (C) Distribution of the expression signals for the indicated genes within the stromal cell cluster. (D) UMAP plots ( fibroXplorer.com ) of mouse lung fibroblasts identified as Dpt+ universal fibroblasts from BLM-treated lungs. Gene expression level for each gene is shown in the fibroblast sub-clusters. Lung fibroblast sub-clusters are color-coded (see left panel). (E) Pre-labeled MDSCs isolated from naïve BM were placed in the upper inserts. Cell-free CMs collected from untreated (control CM) or TGFβ-treated MLF (TGFβ-CM) cultures were incubated with B7H3 blocking antibody (Ab) or control IgG prior to placing in the lower chambers. The fluorescence intensity of the lower chamber was measured at 18 h of incubation. The data are presented as the percentages of TGFβ CMs over their respective control CMs. Mean ± SD are shown. N = 8/group. ****p < 0.0001. scRNA-seq, single-cell RNA sequencing; IPF, idiopathic pulmonary fibrosis; BLM, bleomycin; CMs, conditioned media; MLF, mouse lung fibroblast.

Techniques Used: Expressing, Control, Diffusion-based Assay, Labeling, Gene Expression, Isolation, Incubation, Blocking Assay, Fluorescence, RNA Sequencing

Schematic illustration of the proposed model for B7H3-dependent MDSC role in pulmonary fibrosis. In response to signals from injured lung, hematopoietic progenitor cells (HPCs) proliferate and give rise to myeloid precursors (MPs) under the control of TERT, GM-CSF, and other potential factors. TERT-expressing MP may govern the origination/expansion of MDSCs at intermediate stage of myeloid cell differentiation. Two subtypes of MDSC (G- and M-MDSC) were expanded and activated with the stimulation of GM-CSF/sB7H3 produced by injured lung tissue. The sB7H3-recruited and/or activated MDSCs, in turn, were able to induce resident lung fibroblast activation and/or myofibroblast differentiation through TGFβ production in a paracrine manner and with the greater impact of M-MDSC, thus promoting lung fibrosis. Lung scRNA-seq analysis-identified macrophages and fibroblasts/myofibroblasts were potential cellular sources for induced B7H3 in injured lungs. The findings suggested the potential importance of the observed elevated circulating MDSCs in IPF pathogenesis. In addition, elevated CD84 + suppressive cell-enriched M-MDSC showed some correlation with Tregs in peripheral blood of IPF patients, suggesting MDSC facilitation of immunosuppressive cell network in IPF as well. MDSC, myeloid-derived suppressor cell; TERT, telomerase reverse transcriptase; GM-CSF, granulocyte-macrophage colony-stimulating factor; G-MDSCs, granulocytic myeloid-derived suppressor cells; M-MDSCs, monocytic myeloid-derived suppressor cells; IPF, idiopathic pulmonary fibrosis.

Figure Legend Snippet: Schematic illustration of the proposed model for B7H3-dependent MDSC role in pulmonary fibrosis. In response to signals from injured lung, hematopoietic progenitor cells (HPCs) proliferate and give rise to myeloid precursors (MPs) under the control of TERT, GM-CSF, and other potential factors. TERT-expressing MP may govern the origination/expansion of MDSCs at intermediate stage of myeloid cell differentiation. Two subtypes of MDSC (G- and M-MDSC) were expanded and activated with the stimulation of GM-CSF/sB7H3 produced by injured lung tissue. The sB7H3-recruited and/or activated MDSCs, in turn, were able to induce resident lung fibroblast activation and/or myofibroblast differentiation through TGFβ production in a paracrine manner and with the greater impact of M-MDSC, thus promoting lung fibrosis. Lung scRNA-seq analysis-identified macrophages and fibroblasts/myofibroblasts were potential cellular sources for induced B7H3 in injured lungs. The findings suggested the potential importance of the observed elevated circulating MDSCs in IPF pathogenesis. In addition, elevated CD84 + suppressive cell-enriched M-MDSC showed some correlation with Tregs in peripheral blood of IPF patients, suggesting MDSC facilitation of immunosuppressive cell network in IPF as well. MDSC, myeloid-derived suppressor cell; TERT, telomerase reverse transcriptase; GM-CSF, granulocyte-macrophage colony-stimulating factor; G-MDSCs, granulocytic myeloid-derived suppressor cells; M-MDSCs, monocytic myeloid-derived suppressor cells; IPF, idiopathic pulmonary fibrosis.

Techniques Used: Control, Expressing, Cell Differentiation, Produced, Activation Assay, Derivative Assay, Reverse Transcription

other:

Article Title: Codelivery of apigenin, FdUMP and CD276 antibody synergistic inhibit colorectal cancer by ferroptosis-apoptosis-pyroptosis and CD276 blockade
Article Snippet: CD276 antibody was purchased from BioxCell (USA).

Article Title: Targeting B7-H3 inhibition-induced activation of fatty acid synthesis boosts anti-B7-H3 immunotherapy in triple-negative breast cancer.
Article Snippet: These agents included the B7- H3 mAb (BioXCell, Catalog BE0124), the FASN inhibitor (MCE, HY- 120394), and the PD- L1 mAb (BioXCell, Catalog BE0101).

Staining:

Article Title: Low-affinity binding of anti-B7-H3 clone MJ18 to murine B7-H3 fails to induce tumor regression.
Article Snippet: .. Tumor cell lines and murine splenocytes were stained for flow cytometry assays in FACS buffer (1X PBS, 2 mM EDTA and 2% FBS)57 with the following antibody panel: CD3-BV510 (BioLegend, clone 17A2, cat. 100233), NK1.1-PE-Cy7 (BioLegend, clone PK136, cat. 108713), CD19-FITC (BioLegend, clone 6D5, cat. 115505), F4/80-PE (BioLegend, clone BM8, cat. 123109), B7-H3-AF647 (Abcam, clone EPNCIR122, ab134161), B7-H3-AF647 (BioXcell, clone MJ18, catalog BE0124). .. When indicated, cells were treated with Fc block prior to antibody staining (TruStain FcXTM PLUS (anti-mouse CD16/32) Antibody, BioLegend, San Diego, CA).

Article Title: Low-affinity binding of anti-B7-H3 clone MJ18 to murine B7-H3 fails to induce tumor regression
Article Snippet: .. Tumor cell lines and murine splenocytes were stained for flow cytometry assays in FACS buffer (1X PBS, 2 mM EDTA and 2% FBS) with the following antibody panel: CD3-BV510 (BioLegend, clone 17A2, cat. 100,233), NK1.1-PE-Cy7 (BioLegend, clone PK136, cat. 108,713), CD19-FITC (BioLegend, clone 6D5, cat. 115,505), F4/80-PE (BioLegend, clone BM8, cat. 123,109), B7-H3-AF647 (Abcam, clone EPNCIR122, ab134161), B7-H3-AF647 (BioXcell, clone MJ18, catalog BE0124). .. When indicated, cells were treated with Fc block prior to antibody staining (TruStain FcXTM PLUS (anti-mouse CD16/32) Antibody, BioLegend, San Diego, CA).

Flow Cytometry:

FACS:

In Vivo:

Article Title: Oncogenic activation of SMYD3-SHCBP1 promotes breast cancer development and is coupled with resistance to immune therapy
Article Snippet: GRB2 (C-7) Antibody , Santa Cruz , sc-8034 , , 1:500. .. In Vivo MAb anti-mouse PD-1 (CD276) , BioX Cell , BE0146 , , . .. F4/80 , Abcam , ab6640 , 1:200 , .

Article Title: Tumor-associated Schwann cell remodeling under metabolic stress via lactate sensing orchestrates pancreatic ductal adenocarcinoma development.
Article Snippet: Article Tumor-associated Schwann cell remodeling under metabolic stress via lactate sensing orchestrates pancreatic ductal adenocarcinoma development

Injection:

Article Title: The AURKA inhibitor alters the immune microenvironment and enhances targeting B7-H3 immunotherapy in glioblastoma
Article Snippet: .. For combination therapy, alisertib was administered for 2 days before combination with an i.p. injection of either anti–B7-H3 mAbs (300 μg every 2 days, a total of 4 times; BE01224 clone MJ18, BioXcell) or an isotype control antibody (300 μg every 2 days, a total of 4 times; BE0088, clone HRPN, BioXcell). ..

Control:

Solvent:

Article Title: Dihydropyrrolopyrazole derivative
Article Snippet: The prepared cell suspension was injected under the skin on the right side of the abdomen of C57BL/6 mice (female, supplied by SLC Japan) at 0.1 mL per mouse. .. After a prescribed amount of time had elapsed, the long and short dimensions (mm) of the tumors were with an electronic caliper (Mitutoyo Cat. 500-712-10), and the volumes of the tumors were calculated using the following formula: Tumor volume (mm3)=(long dimension)×(short dimension)×(short dimension)×0.5 Those subjects with tumor volumes the range of 50-200 mm3 were selected and divided into groups with similar tumor volumes, and 250 g/mouse anti-PD-1 antibodies (BioXcell) or 250 g/mouse IgG2a (BioXcell) were administered intraperitoneally, followed by oral administration of the test compound (25 mg/kg or 100 mg/kg) or of the solvent only, to the respective groups. ..

Review