anti cd47 antibodies Search Results


94
Miltenyi Biotec antibodies against cd47
SARS-CoV-2 infection is associated with increased <t>CD47</t> levels. A) TF protein abundance in uninfected (control) and SARS-CoV-2-infected (virus) Caco-2 cells (data derived from . P-values were determined by two-sided Student’s t-test. B) CD47 and SARS-CoV-2 N protein levels and virus titres (genomic RNA determined by PCR) in SARS-CoV-2 strain FFM7 (MOI 1)-infected air-liquid interface cultures of primary human bronchial epithelial (HBE) cells and SARS-CoV-2 strain FFM7 (MOI 0.1)-infected Calu-3 cells. Uncropped blots are provided in Suppl. Figure 1. C) CD47 mRNA levels in post mortem samples from COVID-19 patients (data derived from ). P-values were determined by two-sided Student’s t-test.
Antibodies Against Cd47, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Miltenyi Biotec cd47 pe vio770
BEN-TBI does not result in appreciable donor T-cell phenotypic differences post-transplant when compared to CY-TBI. (a–c) BALB/c recipient mice received 40 mg/kg BEN iv or 200 mg/kg CY ip on day −2, 400 cGy TBI on day −1, and 10 7 TCD-BM from naïve C57BL/6 mice with 3 × 10 6 CellTrace Violet-stained tT from naïve BoyJ mice on day 0. Blood and spleen were collected on day +3. (a) % donor T-cells (CD45.1+) was determined by flow cytometry. Using CBCs determined by HemaVet analysis, absolute number of donor T-cells was calculated. (b) After gating on CD45.1+ cells (representing donor T-cells), CellTrace Violet dilution was analyzed using ModFit software to determine proliferation index. Representative CellTrace Violet dilution is shown. (c) Within the CD45.1+ gate, cells were stratified by CellTrace high (non- proliferative) and CellTrace low (proliferative) and CD25 and <t>CD47</t> expression were analyzed by flow cytometry. Pooled data from 2 experiments with line at mean are shown, n = 6–7 mice/group. * p < .05 , ** p < .01 . (d-g) BALB/c recipient mice received 40 mg/kg BEN iv or 200 mg/kg CY ip on day −2, 400 cGy TBI on day −1, and 10 7 BM with 3 × 10 6 SC from naïve C57BL/6 mice on day 0. Peripheral blood was collected on days +7, +14, +21, +35, and +70 and stained for CD8, CD4, Tbet, GATA3, RORγt, CD134, CD278, PD-1, TIM3, CTLA-4, and CD272. CBCs were determined and used to calculate absolute cell numbers. Average absolute numbers of cells per μL of blood are shown with SEM. Representative flow plots from day +7 with fluorescence minus one (FMO) controls are shown (e). (d) Pooled data from 4 experiments are shown, n = 19 mice/group. (e-g) Pooled data from 2 experiments are shown, n = 10 mice/group. ** p < .01.
Cd47 Pe Vio770, supplied by Miltenyi Biotec, 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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Average 90 stars, based on 1 article reviews
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Cusabio rabbit anti human cd47
BEN-TBI does not result in appreciable donor T-cell phenotypic differences post-transplant when compared to CY-TBI. (a–c) BALB/c recipient mice received 40 mg/kg BEN iv or 200 mg/kg CY ip on day −2, 400 cGy TBI on day −1, and 10 7 TCD-BM from naïve C57BL/6 mice with 3 × 10 6 CellTrace Violet-stained tT from naïve BoyJ mice on day 0. Blood and spleen were collected on day +3. (a) % donor T-cells (CD45.1+) was determined by flow cytometry. Using CBCs determined by HemaVet analysis, absolute number of donor T-cells was calculated. (b) After gating on CD45.1+ cells (representing donor T-cells), CellTrace Violet dilution was analyzed using ModFit software to determine proliferation index. Representative CellTrace Violet dilution is shown. (c) Within the CD45.1+ gate, cells were stratified by CellTrace high (non- proliferative) and CellTrace low (proliferative) and CD25 and <t>CD47</t> expression were analyzed by flow cytometry. Pooled data from 2 experiments with line at mean are shown, n = 6–7 mice/group. * p < .05 , ** p < .01 . (d-g) BALB/c recipient mice received 40 mg/kg BEN iv or 200 mg/kg CY ip on day −2, 400 cGy TBI on day −1, and 10 7 BM with 3 × 10 6 SC from naïve C57BL/6 mice on day 0. Peripheral blood was collected on days +7, +14, +21, +35, and +70 and stained for CD8, CD4, Tbet, GATA3, RORγt, CD134, CD278, PD-1, TIM3, CTLA-4, and CD272. CBCs were determined and used to calculate absolute cell numbers. Average absolute numbers of cells per μL of blood are shown with SEM. Representative flow plots from day +7 with fluorescence minus one (FMO) controls are shown (e). (d) Pooled data from 4 experiments are shown, n = 19 mice/group. (e-g) Pooled data from 2 experiments are shown, n = 10 mice/group. ** p < .01.
Rabbit Anti Human Cd47, supplied by Cusabio, 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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Elabscience Biotechnology pe anti human cd47
BEN-TBI does not result in appreciable donor T-cell phenotypic differences post-transplant when compared to CY-TBI. (a–c) BALB/c recipient mice received 40 mg/kg BEN iv or 200 mg/kg CY ip on day −2, 400 cGy TBI on day −1, and 10 7 TCD-BM from naïve C57BL/6 mice with 3 × 10 6 CellTrace Violet-stained tT from naïve BoyJ mice on day 0. Blood and spleen were collected on day +3. (a) % donor T-cells (CD45.1+) was determined by flow cytometry. Using CBCs determined by HemaVet analysis, absolute number of donor T-cells was calculated. (b) After gating on CD45.1+ cells (representing donor T-cells), CellTrace Violet dilution was analyzed using ModFit software to determine proliferation index. Representative CellTrace Violet dilution is shown. (c) Within the CD45.1+ gate, cells were stratified by CellTrace high (non- proliferative) and CellTrace low (proliferative) and CD25 and <t>CD47</t> expression were analyzed by flow cytometry. Pooled data from 2 experiments with line at mean are shown, n = 6–7 mice/group. * p < .05 , ** p < .01 . (d-g) BALB/c recipient mice received 40 mg/kg BEN iv or 200 mg/kg CY ip on day −2, 400 cGy TBI on day −1, and 10 7 BM with 3 × 10 6 SC from naïve C57BL/6 mice on day 0. Peripheral blood was collected on days +7, +14, +21, +35, and +70 and stained for CD8, CD4, Tbet, GATA3, RORγt, CD134, CD278, PD-1, TIM3, CTLA-4, and CD272. CBCs were determined and used to calculate absolute cell numbers. Average absolute numbers of cells per μL of blood are shown with SEM. Representative flow plots from day +7 with fluorescence minus one (FMO) controls are shown (e). (d) Pooled data from 4 experiments are shown, n = 19 mice/group. (e-g) Pooled data from 2 experiments are shown, n = 10 mice/group. ** p < .01.
Pe Anti Human Cd47, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Elabscience Biotechnology anti human mouse rat cd47 antibody
Preparation and characterization of <t>anti‐CD47‐PCM@NP.</t> A) Hydrodynamic size and zeta potential of CM vesicles, PLGA cores (NP), PCM@NP, and anti‐CD47‐PCM@NP. Data are means ± SD ( n = 3). B) Colocalization of NP/C6 (green) with DiD‐PCM (red), and the colocalization of FITC‐antibody (green) with DiD‐PCM@NP (red), both assessed by confocal laser scanning microscope (CLSM) (scale bar = 5 µm). C) Transmission electron micrographs of (a) NP, (b) CM vesicle, (c) PCM@NP, (d) Anti‐CD47‐PCM@NP, and (e) multiple anti‐CD47‐PCM@NP. All scale bars = 100 nm. D) SDS‐PAGE protein analysis of NP, PCM@NP, CM vesicles, and cancer cell lysate. Samples were tested at equal protein concentrations. CD47 protein and membrane‐specific protein on the cancer cell membrane were efficiently retained on the extracted membrane vesicles and the PCM@NP, detected by western blot. E) Determination of the antibody labeled by PE loaded on the surface of anti‐CD47‐PCM@NP by flow nanoanalyzer. F) The binding affinity of the antibody to the CM vesicles by surface plasmon resonance (SPR).
Anti Human Mouse Rat Cd47 Antibody, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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94
Elabscience Biotechnology anti fitc-labeled cd47
Preparation and characterization of <t>anti‐CD47‐PCM@NP.</t> A) Hydrodynamic size and zeta potential of CM vesicles, PLGA cores (NP), PCM@NP, and anti‐CD47‐PCM@NP. Data are means ± SD ( n = 3). B) Colocalization of NP/C6 (green) with DiD‐PCM (red), and the colocalization of FITC‐antibody (green) with DiD‐PCM@NP (red), both assessed by confocal laser scanning microscope (CLSM) (scale bar = 5 µm). C) Transmission electron micrographs of (a) NP, (b) CM vesicle, (c) PCM@NP, (d) Anti‐CD47‐PCM@NP, and (e) multiple anti‐CD47‐PCM@NP. All scale bars = 100 nm. D) SDS‐PAGE protein analysis of NP, PCM@NP, CM vesicles, and cancer cell lysate. Samples were tested at equal protein concentrations. CD47 protein and membrane‐specific protein on the cancer cell membrane were efficiently retained on the extracted membrane vesicles and the PCM@NP, detected by western blot. E) Determination of the antibody labeled by PE loaded on the surface of anti‐CD47‐PCM@NP by flow nanoanalyzer. F) The binding affinity of the antibody to the CM vesicles by surface plasmon resonance (SPR).
Anti Fitc Labeled Cd47, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Boster Bio rabbit anti cd47
Preparation and characterization of <t>anti‐CD47‐PCM@NP.</t> A) Hydrodynamic size and zeta potential of CM vesicles, PLGA cores (NP), PCM@NP, and anti‐CD47‐PCM@NP. Data are means ± SD ( n = 3). B) Colocalization of NP/C6 (green) with DiD‐PCM (red), and the colocalization of FITC‐antibody (green) with DiD‐PCM@NP (red), both assessed by confocal laser scanning microscope (CLSM) (scale bar = 5 µm). C) Transmission electron micrographs of (a) NP, (b) CM vesicle, (c) PCM@NP, (d) Anti‐CD47‐PCM@NP, and (e) multiple anti‐CD47‐PCM@NP. All scale bars = 100 nm. D) SDS‐PAGE protein analysis of NP, PCM@NP, CM vesicles, and cancer cell lysate. Samples were tested at equal protein concentrations. CD47 protein and membrane‐specific protein on the cancer cell membrane were efficiently retained on the extracted membrane vesicles and the PCM@NP, detected by western blot. E) Determination of the antibody labeled by PE loaded on the surface of anti‐CD47‐PCM@NP by flow nanoanalyzer. F) The binding affinity of the antibody to the CM vesicles by surface plasmon resonance (SPR).
Rabbit Anti Cd47, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Boster Bio rabbit anti human cd47
Preparation and characterization of <t>anti‐CD47‐PCM@NP.</t> A) Hydrodynamic size and zeta potential of CM vesicles, PLGA cores (NP), PCM@NP, and anti‐CD47‐PCM@NP. Data are means ± SD ( n = 3). B) Colocalization of NP/C6 (green) with DiD‐PCM (red), and the colocalization of FITC‐antibody (green) with DiD‐PCM@NP (red), both assessed by confocal laser scanning microscope (CLSM) (scale bar = 5 µm). C) Transmission electron micrographs of (a) NP, (b) CM vesicle, (c) PCM@NP, (d) Anti‐CD47‐PCM@NP, and (e) multiple anti‐CD47‐PCM@NP. All scale bars = 100 nm. D) SDS‐PAGE protein analysis of NP, PCM@NP, CM vesicles, and cancer cell lysate. Samples were tested at equal protein concentrations. CD47 protein and membrane‐specific protein on the cancer cell membrane were efficiently retained on the extracted membrane vesicles and the PCM@NP, detected by western blot. E) Determination of the antibody labeled by PE loaded on the surface of anti‐CD47‐PCM@NP by flow nanoanalyzer. F) The binding affinity of the antibody to the CM vesicles by surface plasmon resonance (SPR).
Rabbit Anti Human Cd47, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+cd47+antibodies/Anti-CD47+Antibody+Picoband/pm38383737-272-45-50
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Boster Bio cd47
Cell differentiation trajectories in CRC obtained by pseudotime analysis. (A–D) tSNE map shows the results of the dimensionality reduction and clustering analysis of S112 (A) , S115 (B) , S114 (C) , and 927 (D) (up). Results of pseudotime cell trajectory in S112 (A) , S115 (B) , S114 (C) , and S927 (D) (down). (E) Twelve genes were screened by invasive modules. (F) The relationship of STC1 expression level and cancer stage/progression-free survival in colon cancer (up) and rectal cancer (down) from TCGA database. (G) The relationship of CES1 expression level and cancer stage in colon cancer (up) and rectal cancer (down) from TCGA database. (H) Immunohistochemical staining showed the expression of AKR1B1(left panel), STC1(middle panel), and <t>CD47(right</t> panel) in Mucosa and cancer(up) and Invasive margin(down) (n=45). The scale bars on the lower right are 100 µm. *P < 0.05, **P < 0.01 and ***P < 0.001. NS, not significant difference.
Cd47, supplied by Boster Bio, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Tioma Therapeutics anti-murine cd47 antibody vx-1000r
Abrogation of CD47 signaling enhances in vivo adaptive immune response to Triple Negative Breast Cancer cell lines in multiple mouse strains. a) In vivo analysis of WT C57Bl/6 mice engrafted with 2*106 EO771 cells with CD47 shRNA KD, a scrambled shRNA control, or CD47 overexpression (OE). b) and c) In vivo analysis of WT Balb/c mice engrafted with 5*105 JC cells with CD47 KD and 104 4T1 cells with CD47 KD, respectively. d) Representative in vivo analysis of C57Bl/6 mice engrafted with 106 EO771-WT cells treated with PBS or the anti-CD47 antibody <t>VX-1000R.</t> N = 10 mice per group for a) and d). N = 5 mice per group for b) and c). Each panel is a representative survival and growth kinetics analysis (panel insert) from one animal study and was repeated at least once with equivalent results. The dotted lines and circle markers indicate mice engrafted with cells expressing the shScramble, solid lines and square markers represent those mice engrafted with cells with CD47 shRNA knockdown, dashed lines and triangle markers indicate mice engrafted with cells with CD47 overexpression.
Anti Murine Cd47 Antibody Vx 1000r, supplied by Tioma Therapeutics, 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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GeneScience Pharmaceuticals Co Ltd gentulizumab monoclonal antibody cd47
The brief history of <t>CD47.</t>
Gentulizumab Monoclonal Antibody Cd47, supplied by GeneScience Pharmaceuticals Co Ltd, 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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Image Search Results


SARS-CoV-2 infection is associated with increased CD47 levels. A) TF protein abundance in uninfected (control) and SARS-CoV-2-infected (virus) Caco-2 cells (data derived from . P-values were determined by two-sided Student’s t-test. B) CD47 and SARS-CoV-2 N protein levels and virus titres (genomic RNA determined by PCR) in SARS-CoV-2 strain FFM7 (MOI 1)-infected air-liquid interface cultures of primary human bronchial epithelial (HBE) cells and SARS-CoV-2 strain FFM7 (MOI 0.1)-infected Calu-3 cells. Uncropped blots are provided in Suppl. Figure 1. C) CD47 mRNA levels in post mortem samples from COVID-19 patients (data derived from ). P-values were determined by two-sided Student’s t-test.

Journal: bioRxiv

Article Title: CD47 as a potential biomarker for the early diagnosis of severe COVID-19

doi: 10.1101/2021.03.01.433404

Figure Lengend Snippet: SARS-CoV-2 infection is associated with increased CD47 levels. A) TF protein abundance in uninfected (control) and SARS-CoV-2-infected (virus) Caco-2 cells (data derived from . P-values were determined by two-sided Student’s t-test. B) CD47 and SARS-CoV-2 N protein levels and virus titres (genomic RNA determined by PCR) in SARS-CoV-2 strain FFM7 (MOI 1)-infected air-liquid interface cultures of primary human bronchial epithelial (HBE) cells and SARS-CoV-2 strain FFM7 (MOI 0.1)-infected Calu-3 cells. Uncropped blots are provided in Suppl. Figure 1. C) CD47 mRNA levels in post mortem samples from COVID-19 patients (data derived from ). P-values were determined by two-sided Student’s t-test.

Article Snippet: Detection occurred by using specific antibodies against CD47 (1:100 dilution, CD47 Antibody, anti-human, Biotin, REAfinityTM, # 130-101-343, Miltenyi Biotec), SARS-CoV-2 N (1:1000 dilution, SARS-CoV-2 Nucleocapsid Antibody, Rabbit MAb, #40143-R019, Sino Biological), and GAPDH (1:1000 dilution, Anti-G3PDH Human Polyclonal Antibody, #2275-PC-100, Trevigen).

Techniques: Infection, Quantitative Proteomics, Control, Virus, Derivative Assay

Results of the PubMed ( https://pubmed.ncbi.nlm.nih.gov ) literature search for “CD47 aging” (A) and “CD47 hypertension” (B). C) Overview figure of the data derived from the literature searches. Age-related increased CD47 levels may contribute to pathogenic conditions associated with severe COVID-19.

Journal: bioRxiv

Article Title: CD47 as a potential biomarker for the early diagnosis of severe COVID-19

doi: 10.1101/2021.03.01.433404

Figure Lengend Snippet: Results of the PubMed ( https://pubmed.ncbi.nlm.nih.gov ) literature search for “CD47 aging” (A) and “CD47 hypertension” (B). C) Overview figure of the data derived from the literature searches. Age-related increased CD47 levels may contribute to pathogenic conditions associated with severe COVID-19.

Article Snippet: Detection occurred by using specific antibodies against CD47 (1:100 dilution, CD47 Antibody, anti-human, Biotin, REAfinityTM, # 130-101-343, Miltenyi Biotec), SARS-CoV-2 N (1:1000 dilution, SARS-CoV-2 Nucleocapsid Antibody, Rabbit MAb, #40143-R019, Sino Biological), and GAPDH (1:1000 dilution, Anti-G3PDH Human Polyclonal Antibody, #2275-PC-100, Trevigen).

Techniques: Derivative Assay

Results of the PubMed ( https://pubmed.ncbi.nlm.nih.gov ) literature search for “CD47 diabetes” (A). B) Overview figure of the data derived from the literature search. Hyperglycaemia- and diabetes-induced increased CD47 levels may contribute to immune escape of SARS-CoV-2-infected cells.

Journal: bioRxiv

Article Title: CD47 as a potential biomarker for the early diagnosis of severe COVID-19

doi: 10.1101/2021.03.01.433404

Figure Lengend Snippet: Results of the PubMed ( https://pubmed.ncbi.nlm.nih.gov ) literature search for “CD47 diabetes” (A). B) Overview figure of the data derived from the literature search. Hyperglycaemia- and diabetes-induced increased CD47 levels may contribute to immune escape of SARS-CoV-2-infected cells.

Article Snippet: Detection occurred by using specific antibodies against CD47 (1:100 dilution, CD47 Antibody, anti-human, Biotin, REAfinityTM, # 130-101-343, Miltenyi Biotec), SARS-CoV-2 N (1:1000 dilution, SARS-CoV-2 Nucleocapsid Antibody, Rabbit MAb, #40143-R019, Sino Biological), and GAPDH (1:1000 dilution, Anti-G3PDH Human Polyclonal Antibody, #2275-PC-100, Trevigen).

Techniques: Derivative Assay, Infection

BEN-TBI does not result in appreciable donor T-cell phenotypic differences post-transplant when compared to CY-TBI. (a–c) BALB/c recipient mice received 40 mg/kg BEN iv or 200 mg/kg CY ip on day −2, 400 cGy TBI on day −1, and 10 7 TCD-BM from naïve C57BL/6 mice with 3 × 10 6 CellTrace Violet-stained tT from naïve BoyJ mice on day 0. Blood and spleen were collected on day +3. (a) % donor T-cells (CD45.1+) was determined by flow cytometry. Using CBCs determined by HemaVet analysis, absolute number of donor T-cells was calculated. (b) After gating on CD45.1+ cells (representing donor T-cells), CellTrace Violet dilution was analyzed using ModFit software to determine proliferation index. Representative CellTrace Violet dilution is shown. (c) Within the CD45.1+ gate, cells were stratified by CellTrace high (non- proliferative) and CellTrace low (proliferative) and CD25 and CD47 expression were analyzed by flow cytometry. Pooled data from 2 experiments with line at mean are shown, n = 6–7 mice/group. * p < .05 , ** p < .01 . (d-g) BALB/c recipient mice received 40 mg/kg BEN iv or 200 mg/kg CY ip on day −2, 400 cGy TBI on day −1, and 10 7 BM with 3 × 10 6 SC from naïve C57BL/6 mice on day 0. Peripheral blood was collected on days +7, +14, +21, +35, and +70 and stained for CD8, CD4, Tbet, GATA3, RORγt, CD134, CD278, PD-1, TIM3, CTLA-4, and CD272. CBCs were determined and used to calculate absolute cell numbers. Average absolute numbers of cells per μL of blood are shown with SEM. Representative flow plots from day +7 with fluorescence minus one (FMO) controls are shown (e). (d) Pooled data from 4 experiments are shown, n = 19 mice/group. (e-g) Pooled data from 2 experiments are shown, n = 10 mice/group. ** p < .01.

Journal: Oncoimmunology

Article Title: Bendamustine with total body irradiation conditioning yields tolerant T-cells while preserving T-cell-dependent graft-versus-leukemia

doi: 10.1080/2162402X.2020.1758011

Figure Lengend Snippet: BEN-TBI does not result in appreciable donor T-cell phenotypic differences post-transplant when compared to CY-TBI. (a–c) BALB/c recipient mice received 40 mg/kg BEN iv or 200 mg/kg CY ip on day −2, 400 cGy TBI on day −1, and 10 7 TCD-BM from naïve C57BL/6 mice with 3 × 10 6 CellTrace Violet-stained tT from naïve BoyJ mice on day 0. Blood and spleen were collected on day +3. (a) % donor T-cells (CD45.1+) was determined by flow cytometry. Using CBCs determined by HemaVet analysis, absolute number of donor T-cells was calculated. (b) After gating on CD45.1+ cells (representing donor T-cells), CellTrace Violet dilution was analyzed using ModFit software to determine proliferation index. Representative CellTrace Violet dilution is shown. (c) Within the CD45.1+ gate, cells were stratified by CellTrace high (non- proliferative) and CellTrace low (proliferative) and CD25 and CD47 expression were analyzed by flow cytometry. Pooled data from 2 experiments with line at mean are shown, n = 6–7 mice/group. * p < .05 , ** p < .01 . (d-g) BALB/c recipient mice received 40 mg/kg BEN iv or 200 mg/kg CY ip on day −2, 400 cGy TBI on day −1, and 10 7 BM with 3 × 10 6 SC from naïve C57BL/6 mice on day 0. Peripheral blood was collected on days +7, +14, +21, +35, and +70 and stained for CD8, CD4, Tbet, GATA3, RORγt, CD134, CD278, PD-1, TIM3, CTLA-4, and CD272. CBCs were determined and used to calculate absolute cell numbers. Average absolute numbers of cells per μL of blood are shown with SEM. Representative flow plots from day +7 with fluorescence minus one (FMO) controls are shown (e). (d) Pooled data from 4 experiments are shown, n = 19 mice/group. (e-g) Pooled data from 2 experiments are shown, n = 10 mice/group. ** p < .01.

Article Snippet: Antibodies used were anti-mouse H2kb PerCP-eFluor710 (clone AF6-88.5.5.3; 46–5958), CD8α PE-Cy7 (53–6.7; 25–0081), CD4 APC (RM4-5; 50-148-54), FoxP3 APC (FJK-16s; 17–5773), CD45.1 APC (A20; 17–0453), GATA3 PE-Cy7 (TWAJ; 25–9966), CD134 PE-Cy7 (OX-86; 25–1341), FoxP3 PE (150D/E4; 12–4774), CD69 PE-Cy5 (H1.2F3; 15–0691), RORγt APC (AFKJS-9; 17–6988), IFN gamma PE (XMG1.2, 12–7311) (Thermo Fisher Scientific), CD45.1 PE-CF594 (A20; 562452), CD3ε PE-CF594 (145–2 C11; 562286), CD44 BB515 (IM7; 565941), CD44 BV510 (IM7; 563114) (BD Biosciences), CD47 PE-Vio770 (REA170; 130-102-383), TIM-3 VioBright FITC (REA602; 130-109-449), TIM-3 PE (REA602; 130-118-563), CD278 VioGreen (REA192; 130-100-739), CD272 PE (REA224; 130-102-689), CD4 APC-Vio770 (GK1.5; 130-102-786), CD4 VioGreen (GK1.5; 130-102-444) (Miltenyi Biotec), Tbet PE-Dazzle594 (4B10; 644828), CTLA-4 PE-Dazzle594 (UC10-4B9; 106318), CD8α Brilliant Violet 421 (53–6.7; 100738), CCR7 PE-Cy5 (4B12; 120114), PD-1 APC (29F.1A12; 135210), CD25 AlexaFluor700 (PC61; 102024), and TNF-α Brilliant Violet 510 (MP6-XT22, 506339) (Biolegend).

Techniques: Staining, Flow Cytometry, Software, Expressing, Fluorescence

Preparation and characterization of anti‐CD47‐PCM@NP. A) Hydrodynamic size and zeta potential of CM vesicles, PLGA cores (NP), PCM@NP, and anti‐CD47‐PCM@NP. Data are means ± SD ( n = 3). B) Colocalization of NP/C6 (green) with DiD‐PCM (red), and the colocalization of FITC‐antibody (green) with DiD‐PCM@NP (red), both assessed by confocal laser scanning microscope (CLSM) (scale bar = 5 µm). C) Transmission electron micrographs of (a) NP, (b) CM vesicle, (c) PCM@NP, (d) Anti‐CD47‐PCM@NP, and (e) multiple anti‐CD47‐PCM@NP. All scale bars = 100 nm. D) SDS‐PAGE protein analysis of NP, PCM@NP, CM vesicles, and cancer cell lysate. Samples were tested at equal protein concentrations. CD47 protein and membrane‐specific protein on the cancer cell membrane were efficiently retained on the extracted membrane vesicles and the PCM@NP, detected by western blot. E) Determination of the antibody labeled by PE loaded on the surface of anti‐CD47‐PCM@NP by flow nanoanalyzer. F) The binding affinity of the antibody to the CM vesicles by surface plasmon resonance (SPR).

Journal: Advanced Science

Article Title: Overcoming the On‐Target Toxicity in Antibody‐Mediated Therapies via an Indirect Active Targeting Strategy

doi: 10.1002/advs.202206912

Figure Lengend Snippet: Preparation and characterization of anti‐CD47‐PCM@NP. A) Hydrodynamic size and zeta potential of CM vesicles, PLGA cores (NP), PCM@NP, and anti‐CD47‐PCM@NP. Data are means ± SD ( n = 3). B) Colocalization of NP/C6 (green) with DiD‐PCM (red), and the colocalization of FITC‐antibody (green) with DiD‐PCM@NP (red), both assessed by confocal laser scanning microscope (CLSM) (scale bar = 5 µm). C) Transmission electron micrographs of (a) NP, (b) CM vesicle, (c) PCM@NP, (d) Anti‐CD47‐PCM@NP, and (e) multiple anti‐CD47‐PCM@NP. All scale bars = 100 nm. D) SDS‐PAGE protein analysis of NP, PCM@NP, CM vesicles, and cancer cell lysate. Samples were tested at equal protein concentrations. CD47 protein and membrane‐specific protein on the cancer cell membrane were efficiently retained on the extracted membrane vesicles and the PCM@NP, detected by western blot. E) Determination of the antibody labeled by PE loaded on the surface of anti‐CD47‐PCM@NP by flow nanoanalyzer. F) The binding affinity of the antibody to the CM vesicles by surface plasmon resonance (SPR).

Article Snippet: The cells were diluted at 1× 10 6 cells per mL in a culture medium and incubated with 1.0 mg mL −1 of a PE anti‐human/mouse/rat CD47 antibody (E‐AB‐F1016D, Elabscience) or anti‐Neu/ErbB2/HER2 Antibody (SC‐7301, Santa Cruz Biotechnology) and CoraLite488‐conjugated Affinipure coat anti‐mouse IgG(H+L) (SA00013‐1, Proteintech) for 30 min at 4 °C.

Techniques: Zeta Potential Analyzer, Laser-Scanning Microscopy, Transmission Assay, SDS Page, Membrane, Western Blot, Labeling, Binding Assay, SPR Assay

Anti‐CD47‐PCM@NP effectively distinguished target cells from CD47‐expressing nontarget cells in vitro through indirect active targeting. A) Anti‐CD47‐PCM@NP avoided the blocking of CD47 on RBC and subsequent phagocytosis thus circumvented the on‐target toxicity of free anti‐CD47 towards RBC through the INTACT strategy. Scale bar = 50 µm. B,C) PCM@NP and anti‐CD47‐PCM@NP efficiently escaped the capture by B) macrophages with enhanced and parallel cellular uptake by C) target 4T1 cells, measured by flow cytometry. The antibody selectively dissociated from the carrier PCM@NP at the presence of 4T1 cells with high expression of D) CD47 in contrast to E) CD47 −/− 4T1 cells, shown by colocalization images and distribution map of PE‐antibody (red) and PCM@NP/C6 (green). Scale bar = 20 µm (multi‐cell images), 2 µm (single‐cell images). F) The schematic diagram of the microfluidic device. The tumor cells were cultured in the cavity of the microfluidic chip till adherence, and then exposed to flowing anti‐CD47 or anti‐CD47‐PCM@NP, and fluorescent images were captured at predetermined time points. G) Free anti‐CD47 sufficiently bound to the surface of 4T1 cells with high expression of CD47 (a). The antibody dissociated from PCM@NP at the presence of 4T1 cells (b), in contrast with CD47 −/− 4T1 group (c) (antibody labeled with FITC, green. PCM@NP labeled with DiD, red). Scale bar = 10 µm. Original movies are shown in Movie S1 (Supporting Information) (a), Movie S2 (Supporting Information) (b), and Movie S3 (Supporting Information) (c), respectively. Data are presented as mean ± SD ( n = 3). (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; NS represents non‐significance).

Journal: Advanced Science

Article Title: Overcoming the On‐Target Toxicity in Antibody‐Mediated Therapies via an Indirect Active Targeting Strategy

doi: 10.1002/advs.202206912

Figure Lengend Snippet: Anti‐CD47‐PCM@NP effectively distinguished target cells from CD47‐expressing nontarget cells in vitro through indirect active targeting. A) Anti‐CD47‐PCM@NP avoided the blocking of CD47 on RBC and subsequent phagocytosis thus circumvented the on‐target toxicity of free anti‐CD47 towards RBC through the INTACT strategy. Scale bar = 50 µm. B,C) PCM@NP and anti‐CD47‐PCM@NP efficiently escaped the capture by B) macrophages with enhanced and parallel cellular uptake by C) target 4T1 cells, measured by flow cytometry. The antibody selectively dissociated from the carrier PCM@NP at the presence of 4T1 cells with high expression of D) CD47 in contrast to E) CD47 −/− 4T1 cells, shown by colocalization images and distribution map of PE‐antibody (red) and PCM@NP/C6 (green). Scale bar = 20 µm (multi‐cell images), 2 µm (single‐cell images). F) The schematic diagram of the microfluidic device. The tumor cells were cultured in the cavity of the microfluidic chip till adherence, and then exposed to flowing anti‐CD47 or anti‐CD47‐PCM@NP, and fluorescent images were captured at predetermined time points. G) Free anti‐CD47 sufficiently bound to the surface of 4T1 cells with high expression of CD47 (a). The antibody dissociated from PCM@NP at the presence of 4T1 cells (b), in contrast with CD47 −/− 4T1 group (c) (antibody labeled with FITC, green. PCM@NP labeled with DiD, red). Scale bar = 10 µm. Original movies are shown in Movie S1 (Supporting Information) (a), Movie S2 (Supporting Information) (b), and Movie S3 (Supporting Information) (c), respectively. Data are presented as mean ± SD ( n = 3). (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; NS represents non‐significance).

Article Snippet: The cells were diluted at 1× 10 6 cells per mL in a culture medium and incubated with 1.0 mg mL −1 of a PE anti‐human/mouse/rat CD47 antibody (E‐AB‐F1016D, Elabscience) or anti‐Neu/ErbB2/HER2 Antibody (SC‐7301, Santa Cruz Biotechnology) and CoraLite488‐conjugated Affinipure coat anti‐mouse IgG(H+L) (SA00013‐1, Proteintech) for 30 min at 4 °C.

Techniques: Expressing, In Vitro, Blocking Assay, Flow Cytometry, Cell Culture, Labeling

Evaluation of the biological functions of anti‐CD47‐PCM@NP in vivo. A) In vivo and ex vivo targeting ability of anti‐CD47‐PCM@NP and anti‐CD47 in tumor‐bearing mice models determined by live imaging. B) The semiquantitative analysis of the ratio of fluorescence intensity (tumor/liver) of ex vivo imaging. C) In vivo biodistribution of coumarin 6 (C6)‐labeled formulations in tumor‐bearing mice models at (a) 2 h, (b) 4 h, (c) 8 h, and (d) 12 h after i.v. injection of NP/C6, PCM@NP/C6 and anti‐CD47‐PCM@NP/C6. Data are presented as mean ± SD ( n = 3) (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; NS represents non‐significance).

Journal: Advanced Science

Article Title: Overcoming the On‐Target Toxicity in Antibody‐Mediated Therapies via an Indirect Active Targeting Strategy

doi: 10.1002/advs.202206912

Figure Lengend Snippet: Evaluation of the biological functions of anti‐CD47‐PCM@NP in vivo. A) In vivo and ex vivo targeting ability of anti‐CD47‐PCM@NP and anti‐CD47 in tumor‐bearing mice models determined by live imaging. B) The semiquantitative analysis of the ratio of fluorescence intensity (tumor/liver) of ex vivo imaging. C) In vivo biodistribution of coumarin 6 (C6)‐labeled formulations in tumor‐bearing mice models at (a) 2 h, (b) 4 h, (c) 8 h, and (d) 12 h after i.v. injection of NP/C6, PCM@NP/C6 and anti‐CD47‐PCM@NP/C6. Data are presented as mean ± SD ( n = 3) (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; NS represents non‐significance).

Article Snippet: The cells were diluted at 1× 10 6 cells per mL in a culture medium and incubated with 1.0 mg mL −1 of a PE anti‐human/mouse/rat CD47 antibody (E‐AB‐F1016D, Elabscience) or anti‐Neu/ErbB2/HER2 Antibody (SC‐7301, Santa Cruz Biotechnology) and CoraLite488‐conjugated Affinipure coat anti‐mouse IgG(H+L) (SA00013‐1, Proteintech) for 30 min at 4 °C.

Techniques: In Vivo, Ex Vivo, Imaging, Fluorescence, Labeling, Injection

Antitumor efficacy of anti‐CD47‐PCM@NP and mechanistic investigation by CyTOF analysis. A) Representative images and phagocytic index of C57BL/6 bone marrow‐derived macrophages (BMDM) phagocytosing tumor cells following treatment with PCM@NP, anti‐CD47, and anti‐CD47‐PCM@NP. Scale bar = 50 µm. B) Timeline of the anti‐tumor efficacy study on tumor‐bearing mice (red arrows indicate intravenous administrations), and average tumor growth curves and picture of tumor tissues after the treatment. C) Individual tumor growth curves in each group. D) viSNE plot of intratumoral cells in tumor tissues after treatment with saline, PCM@NP, anti‐CD47, anti‐CD47‐PCM@NP and all groups merged. E) Heat map of the surface molecule and functional molecule expression of different subsets of immune cells in tumor tissues from all groups merged. F) tSNE visualization of all samples with the expression of CD4 and CD8a respectively. G) Percentage of cells in each cluster after treatment from each group. Data represented as mean ± SD ( n = 6). (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; NS represents nonsignificance).

Journal: Advanced Science

Article Title: Overcoming the On‐Target Toxicity in Antibody‐Mediated Therapies via an Indirect Active Targeting Strategy

doi: 10.1002/advs.202206912

Figure Lengend Snippet: Antitumor efficacy of anti‐CD47‐PCM@NP and mechanistic investigation by CyTOF analysis. A) Representative images and phagocytic index of C57BL/6 bone marrow‐derived macrophages (BMDM) phagocytosing tumor cells following treatment with PCM@NP, anti‐CD47, and anti‐CD47‐PCM@NP. Scale bar = 50 µm. B) Timeline of the anti‐tumor efficacy study on tumor‐bearing mice (red arrows indicate intravenous administrations), and average tumor growth curves and picture of tumor tissues after the treatment. C) Individual tumor growth curves in each group. D) viSNE plot of intratumoral cells in tumor tissues after treatment with saline, PCM@NP, anti‐CD47, anti‐CD47‐PCM@NP and all groups merged. E) Heat map of the surface molecule and functional molecule expression of different subsets of immune cells in tumor tissues from all groups merged. F) tSNE visualization of all samples with the expression of CD4 and CD8a respectively. G) Percentage of cells in each cluster after treatment from each group. Data represented as mean ± SD ( n = 6). (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; NS represents nonsignificance).

Article Snippet: The cells were diluted at 1× 10 6 cells per mL in a culture medium and incubated with 1.0 mg mL −1 of a PE anti‐human/mouse/rat CD47 antibody (E‐AB‐F1016D, Elabscience) or anti‐Neu/ErbB2/HER2 Antibody (SC‐7301, Santa Cruz Biotechnology) and CoraLite488‐conjugated Affinipure coat anti‐mouse IgG(H+L) (SA00013‐1, Proteintech) for 30 min at 4 °C.

Techniques: Derivative Assay, Saline, Functional Assay, Expressing

The INTACT strategy efficiently delivers antibodies to tumors with reduced in vivo toxicity. A) Anti‐CD47‐PCM@NP exhibited no significant influence on red blood cell (RBC), hemoglobin (HGB), hematocrit (HCT), and platelet (PLT). Data represented as mean ± SD ( n = 3). B–D) Anti‐CD47‐PCM@NP relieved the occurrence of fungal infection during antitumor treatment. B) Experimental timeline and treatments in tumor‐bearing mice (arrows indicate intravenous administrations). At day 14, mice were infected with C. albicans via tail vein injection. C) Colony‐forming units (CFU) on day 7 in the kidneys of infected mouse models ( n = 6). D) The survival rates of infected mice with different treatments ( n = 12). Data represented as mean ± SD. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; NS represents non‐significance).

Journal: Advanced Science

Article Title: Overcoming the On‐Target Toxicity in Antibody‐Mediated Therapies via an Indirect Active Targeting Strategy

doi: 10.1002/advs.202206912

Figure Lengend Snippet: The INTACT strategy efficiently delivers antibodies to tumors with reduced in vivo toxicity. A) Anti‐CD47‐PCM@NP exhibited no significant influence on red blood cell (RBC), hemoglobin (HGB), hematocrit (HCT), and platelet (PLT). Data represented as mean ± SD ( n = 3). B–D) Anti‐CD47‐PCM@NP relieved the occurrence of fungal infection during antitumor treatment. B) Experimental timeline and treatments in tumor‐bearing mice (arrows indicate intravenous administrations). At day 14, mice were infected with C. albicans via tail vein injection. C) Colony‐forming units (CFU) on day 7 in the kidneys of infected mouse models ( n = 6). D) The survival rates of infected mice with different treatments ( n = 12). Data represented as mean ± SD. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; NS represents non‐significance).

Article Snippet: The cells were diluted at 1× 10 6 cells per mL in a culture medium and incubated with 1.0 mg mL −1 of a PE anti‐human/mouse/rat CD47 antibody (E‐AB‐F1016D, Elabscience) or anti‐Neu/ErbB2/HER2 Antibody (SC‐7301, Santa Cruz Biotechnology) and CoraLite488‐conjugated Affinipure coat anti‐mouse IgG(H+L) (SA00013‐1, Proteintech) for 30 min at 4 °C.

Techniques: In Vivo, Infection, Injection

The INTACT strategy is adaptive to multiple antibody‐based systems. A) Relative tumor volume growth with anti‐CD47‐PCM@NP/PTX treatment ( n = 6). B–G) The INTACT therapy refined the targeting precision of ADC. B) The diagram of ADC construction: Anti‐CD47 was modified with streptavidin and conjugated with DM1 via the crosslinker BMCC‐biotin. C) The conjugation of ADC was confirmed with SDS‐PAGE. D) Experimental timeline for the anti‐tumor efficacy study and hematology assessments of ADC‐PCM@NP (red arrows indicate intravenous administrations). E) Average tumor growth curves, and picture of the tumor tissues after the treatment ( n = 6). F) Individual tumor growth curves in each group ( n = 6). G) Hematology assessments of red blood cell (RBC), hemoglobin (HGB), hematocrit (HCT), and platelet (PLT) ( n = 3). Data represented as mean ± SD. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; NS represents non‐significance).

Journal: Advanced Science

Article Title: Overcoming the On‐Target Toxicity in Antibody‐Mediated Therapies via an Indirect Active Targeting Strategy

doi: 10.1002/advs.202206912

Figure Lengend Snippet: The INTACT strategy is adaptive to multiple antibody‐based systems. A) Relative tumor volume growth with anti‐CD47‐PCM@NP/PTX treatment ( n = 6). B–G) The INTACT therapy refined the targeting precision of ADC. B) The diagram of ADC construction: Anti‐CD47 was modified with streptavidin and conjugated with DM1 via the crosslinker BMCC‐biotin. C) The conjugation of ADC was confirmed with SDS‐PAGE. D) Experimental timeline for the anti‐tumor efficacy study and hematology assessments of ADC‐PCM@NP (red arrows indicate intravenous administrations). E) Average tumor growth curves, and picture of the tumor tissues after the treatment ( n = 6). F) Individual tumor growth curves in each group ( n = 6). G) Hematology assessments of red blood cell (RBC), hemoglobin (HGB), hematocrit (HCT), and platelet (PLT) ( n = 3). Data represented as mean ± SD. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; NS represents non‐significance).

Article Snippet: The cells were diluted at 1× 10 6 cells per mL in a culture medium and incubated with 1.0 mg mL −1 of a PE anti‐human/mouse/rat CD47 antibody (E‐AB‐F1016D, Elabscience) or anti‐Neu/ErbB2/HER2 Antibody (SC‐7301, Santa Cruz Biotechnology) and CoraLite488‐conjugated Affinipure coat anti‐mouse IgG(H+L) (SA00013‐1, Proteintech) for 30 min at 4 °C.

Techniques: Modification, Conjugation Assay, SDS Page

Cell differentiation trajectories in CRC obtained by pseudotime analysis. (A–D) tSNE map shows the results of the dimensionality reduction and clustering analysis of S112 (A) , S115 (B) , S114 (C) , and 927 (D) (up). Results of pseudotime cell trajectory in S112 (A) , S115 (B) , S114 (C) , and S927 (D) (down). (E) Twelve genes were screened by invasive modules. (F) The relationship of STC1 expression level and cancer stage/progression-free survival in colon cancer (up) and rectal cancer (down) from TCGA database. (G) The relationship of CES1 expression level and cancer stage in colon cancer (up) and rectal cancer (down) from TCGA database. (H) Immunohistochemical staining showed the expression of AKR1B1(left panel), STC1(middle panel), and CD47(right panel) in Mucosa and cancer(up) and Invasive margin(down) (n=45). The scale bars on the lower right are 100 µm. *P < 0.05, **P < 0.01 and ***P < 0.001. NS, not significant difference.

Journal: Frontiers in Oncology

Article Title: Spatially resolved transcriptomics revealed local invasion-related genes in colorectal cancer

doi: 10.3389/fonc.2023.1089090

Figure Lengend Snippet: Cell differentiation trajectories in CRC obtained by pseudotime analysis. (A–D) tSNE map shows the results of the dimensionality reduction and clustering analysis of S112 (A) , S115 (B) , S114 (C) , and 927 (D) (up). Results of pseudotime cell trajectory in S112 (A) , S115 (B) , S114 (C) , and S927 (D) (down). (E) Twelve genes were screened by invasive modules. (F) The relationship of STC1 expression level and cancer stage/progression-free survival in colon cancer (up) and rectal cancer (down) from TCGA database. (G) The relationship of CES1 expression level and cancer stage in colon cancer (up) and rectal cancer (down) from TCGA database. (H) Immunohistochemical staining showed the expression of AKR1B1(left panel), STC1(middle panel), and CD47(right panel) in Mucosa and cancer(up) and Invasive margin(down) (n=45). The scale bars on the lower right are 100 µm. *P < 0.05, **P < 0.01 and ***P < 0.001. NS, not significant difference.

Article Snippet: Antibodies used include STC1 (1:50; Proteintech, China), RPL5(1:800; Proteintech, China), AKR1B1(1:50; BOSTER, China), HLA-A(1:100; BOSTER, China) and CD47(1:400; BOSTER, China).

Techniques: Cell Differentiation, Expressing, Immunohistochemical staining, Staining

Abrogation of CD47 signaling enhances in vivo adaptive immune response to Triple Negative Breast Cancer cell lines in multiple mouse strains. a) In vivo analysis of WT C57Bl/6 mice engrafted with 2*106 EO771 cells with CD47 shRNA KD, a scrambled shRNA control, or CD47 overexpression (OE). b) and c) In vivo analysis of WT Balb/c mice engrafted with 5*105 JC cells with CD47 KD and 104 4T1 cells with CD47 KD, respectively. d) Representative in vivo analysis of C57Bl/6 mice engrafted with 106 EO771-WT cells treated with PBS or the anti-CD47 antibody VX-1000R. N = 10 mice per group for a) and d). N = 5 mice per group for b) and c). Each panel is a representative survival and growth kinetics analysis (panel insert) from one animal study and was repeated at least once with equivalent results. The dotted lines and circle markers indicate mice engrafted with cells expressing the shScramble, solid lines and square markers represent those mice engrafted with cells with CD47 shRNA knockdown, dashed lines and triangle markers indicate mice engrafted with cells with CD47 overexpression.

Journal: Cancer immunology, immunotherapy : CII

Article Title: An unbiased in vivo functional genomics screening approach in mice identifies novel tumor cell-based regulators of immune rejection

doi: 10.1007/s00262-017-2047-2

Figure Lengend Snippet: Abrogation of CD47 signaling enhances in vivo adaptive immune response to Triple Negative Breast Cancer cell lines in multiple mouse strains. a) In vivo analysis of WT C57Bl/6 mice engrafted with 2*106 EO771 cells with CD47 shRNA KD, a scrambled shRNA control, or CD47 overexpression (OE). b) and c) In vivo analysis of WT Balb/c mice engrafted with 5*105 JC cells with CD47 KD and 104 4T1 cells with CD47 KD, respectively. d) Representative in vivo analysis of C57Bl/6 mice engrafted with 106 EO771-WT cells treated with PBS or the anti-CD47 antibody VX-1000R. N = 10 mice per group for a) and d). N = 5 mice per group for b) and c). Each panel is a representative survival and growth kinetics analysis (panel insert) from one animal study and was repeated at least once with equivalent results. The dotted lines and circle markers indicate mice engrafted with cells expressing the shScramble, solid lines and square markers represent those mice engrafted with cells with CD47 shRNA knockdown, dashed lines and triangle markers indicate mice engrafted with cells with CD47 overexpression.

Article Snippet: Anti-CD47 Antibody In Vivo Study The antagonistic anti-murine CD47 antibody, VX-1000R, was provided by Tioma Therapeutics, Inc. (St. Louis, MO) for preclinical testing in our in vivo model system.

Techniques: In Vivo, shRNA, Control, Over Expression, Expressing, Knockdown

The brief history of CD47.

Journal: Journal of Advanced Research

Article Title: Deciphering the role of CD47 in cancer immunotherapy

doi: 10.1016/j.jare.2023.10.009

Figure Lengend Snippet: The brief history of CD47.

Article Snippet: GeneScience , Gentulizumab , Monoclonal Antibody , CD47 , Solid Tumor/NHL , Phase 1 , , single-drug therapy , NCT05221385.

Techniques:

CD47 ligand proteins a CD47 structure and its ligand proteins b SIRP family members c Binding of CD47 on the surface of HSCs and RBCs and SIRPα on macrophages prevents them from phagocytosis by macrophages d CD47 on tumor cells binds to SIRPα on macrophages to protect tumor cells from being phagocytized by macrophages, blocking CD47 by antibody or interrupting the CD47-SIRPα axis promotes phagocytosis and tumor clearance.

Journal: Journal of Advanced Research

Article Title: Deciphering the role of CD47 in cancer immunotherapy

doi: 10.1016/j.jare.2023.10.009

Figure Lengend Snippet: CD47 ligand proteins a CD47 structure and its ligand proteins b SIRP family members c Binding of CD47 on the surface of HSCs and RBCs and SIRPα on macrophages prevents them from phagocytosis by macrophages d CD47 on tumor cells binds to SIRPα on macrophages to protect tumor cells from being phagocytized by macrophages, blocking CD47 by antibody or interrupting the CD47-SIRPα axis promotes phagocytosis and tumor clearance.

Article Snippet: GeneScience , Gentulizumab , Monoclonal Antibody , CD47 , Solid Tumor/NHL , Phase 1 , , single-drug therapy , NCT05221385.

Techniques: Binding Assay, Blocking Assay

Comprehensive list of  CD47  associated/interacted proteins and their major functions.

Journal: Journal of Advanced Research

Article Title: Deciphering the role of CD47 in cancer immunotherapy

doi: 10.1016/j.jare.2023.10.009

Figure Lengend Snippet: Comprehensive list of CD47 associated/interacted proteins and their major functions.

Article Snippet: GeneScience , Gentulizumab , Monoclonal Antibody , CD47 , Solid Tumor/NHL , Phase 1 , , single-drug therapy , NCT05221385.

Techniques: Inhibition, Migration, Cell Function Assay, Activation Assay, Membrane, Binding Assay, Activity Assay, Phospho-proteomics

Regulation and modification of CD47 expression a Regulators of CD47 expression in cancer cells. TNF-α, IL-1β and HER2 can stimulate the expression of CD47 via activating NF-κB pathway. IL-6 increases the expression of CD47 by activating the STAT3 signaling pathway. IFN-γ up-regulates the expression of CD47 via the STAT1-IRF1 signaling pathway. HIF-1 directly binds to the CD47 promoter to promote the transcriptional expression of CD47 in a hypoxic environment. Myc also binds to the CD47 promoter directly to up-regulate CD47 expression. Pyroglutamylation of CD47 protein catalyzed by QPCTL is critical for the binding of CD47-SIRPα and then influences the immune response of macrophages. b Pyroglutamylation of CD47 c Predicted ubiquitination of CD47, ubiquitination sites listed here are the potential sites predicted in the phosphosite website. d N-glycosylation of CD47 e O-glycosylation of CD47.

Journal: Journal of Advanced Research

Article Title: Deciphering the role of CD47 in cancer immunotherapy

doi: 10.1016/j.jare.2023.10.009

Figure Lengend Snippet: Regulation and modification of CD47 expression a Regulators of CD47 expression in cancer cells. TNF-α, IL-1β and HER2 can stimulate the expression of CD47 via activating NF-κB pathway. IL-6 increases the expression of CD47 by activating the STAT3 signaling pathway. IFN-γ up-regulates the expression of CD47 via the STAT1-IRF1 signaling pathway. HIF-1 directly binds to the CD47 promoter to promote the transcriptional expression of CD47 in a hypoxic environment. Myc also binds to the CD47 promoter directly to up-regulate CD47 expression. Pyroglutamylation of CD47 protein catalyzed by QPCTL is critical for the binding of CD47-SIRPα and then influences the immune response of macrophages. b Pyroglutamylation of CD47 c Predicted ubiquitination of CD47, ubiquitination sites listed here are the potential sites predicted in the phosphosite website. d N-glycosylation of CD47 e O-glycosylation of CD47.

Article Snippet: GeneScience , Gentulizumab , Monoclonal Antibody , CD47 , Solid Tumor/NHL , Phase 1 , , single-drug therapy , NCT05221385.

Techniques: Modification, Expressing, Binding Assay, Ubiquitin Proteomics, Phospho-proteomics, Glycoproteomics

MiRNAs regulate  CD47  expression.

Journal: Journal of Advanced Research

Article Title: Deciphering the role of CD47 in cancer immunotherapy

doi: 10.1016/j.jare.2023.10.009

Figure Lengend Snippet: MiRNAs regulate CD47 expression.

Article Snippet: GeneScience , Gentulizumab , Monoclonal Antibody , CD47 , Solid Tumor/NHL , Phase 1 , , single-drug therapy , NCT05221385.

Techniques: Expressing, Binding Assay, Blocking Assay, Transfection, Inhibition, Transduction

CD47 in innate immunity and adaptive immunity a . CD47 on DC regulates its migration and CD47 inhibits the transformation of immature DC to mature DC. b . CD47 on T cells binds with SIRPα on dendritic cells to inhibit the activation of dendritic cells, secretion of cytokines, and negatively regulate T cell expression. c. The interaction of TSP-1 and CD47 induces DC to apoptosis. d . CD47 high expression on NK cells promotes NK recruitment and activation in the TME, and CD47 deficiency on NK cells inhibits above activities. e . The CD47 ligand protein TSP-1 inhibits NK cell proliferation by binding CD47. CD47 regulates NK cell recruitment and activation. Targeting CD47 by antibody miap301 blocks the binding between TSP-1 and CD47 and enhances NK cell’s proliferation. f. CD47 modulates dysregulated neutrophil transmigration across epithelial surfaces. CD47 associates with leukocyte-specific integrin CD11b/CD18 in the plasma membrane of neutrophils, and the loss of CD47 results in impaired CD11b/CD18 activation. g . CD47 plays an essential role in the migration of neutrophils to the injured site. CD47 on the epithelial cells binding with SIPRα on the neutrophils regulates the adhesion function of neutrophils and helps them infiltrate into the tissue space through vascular endothelium. Disrupting CD47 or its binding signal pathway reduces neutrophils’ migration and infiltration. h . TSP-1 on T cell inhibits its activation, and the interaction of TSP-1 and CD47 on T cell promotes naïve T cells differentiation to regulatory T cells. i . Targeting CD47 by antibodies such as Ad22 induces T cell apoptosis promptly, and this process can be completed without TNFRI/p55, TNFRII/p75 or Fas signal pathway. j . By binding CD47, SIRPα enhances T cell proliferation and activates T cell. This may probably be due to the adhesion between T cell and APC cell together with TCR signal transduction. Inhibition of SIRPα and CD47 mAb reduces the proliferation of T lymphocytes. k . Blocking the interaction of CD47 on naïve T cells with TSP-1 prompts the generation of Tregs. l . The interaction between CD47 on B cell and SIRPα on macrophage and DC brings cell–cell interaction which is important to B cell maturation. m . CD19 and BCR co-transduce B cell signal to promote B cell activation and proliferation. The bispecific antibody targeting both CD19 and CD47 inhibits CD19 cluster to move to BCR and inhibits B cell proliferation finally.

Journal: Journal of Advanced Research

Article Title: Deciphering the role of CD47 in cancer immunotherapy

doi: 10.1016/j.jare.2023.10.009

Figure Lengend Snippet: CD47 in innate immunity and adaptive immunity a . CD47 on DC regulates its migration and CD47 inhibits the transformation of immature DC to mature DC. b . CD47 on T cells binds with SIRPα on dendritic cells to inhibit the activation of dendritic cells, secretion of cytokines, and negatively regulate T cell expression. c. The interaction of TSP-1 and CD47 induces DC to apoptosis. d . CD47 high expression on NK cells promotes NK recruitment and activation in the TME, and CD47 deficiency on NK cells inhibits above activities. e . The CD47 ligand protein TSP-1 inhibits NK cell proliferation by binding CD47. CD47 regulates NK cell recruitment and activation. Targeting CD47 by antibody miap301 blocks the binding between TSP-1 and CD47 and enhances NK cell’s proliferation. f. CD47 modulates dysregulated neutrophil transmigration across epithelial surfaces. CD47 associates with leukocyte-specific integrin CD11b/CD18 in the plasma membrane of neutrophils, and the loss of CD47 results in impaired CD11b/CD18 activation. g . CD47 plays an essential role in the migration of neutrophils to the injured site. CD47 on the epithelial cells binding with SIPRα on the neutrophils regulates the adhesion function of neutrophils and helps them infiltrate into the tissue space through vascular endothelium. Disrupting CD47 or its binding signal pathway reduces neutrophils’ migration and infiltration. h . TSP-1 on T cell inhibits its activation, and the interaction of TSP-1 and CD47 on T cell promotes naïve T cells differentiation to regulatory T cells. i . Targeting CD47 by antibodies such as Ad22 induces T cell apoptosis promptly, and this process can be completed without TNFRI/p55, TNFRII/p75 or Fas signal pathway. j . By binding CD47, SIRPα enhances T cell proliferation and activates T cell. This may probably be due to the adhesion between T cell and APC cell together with TCR signal transduction. Inhibition of SIRPα and CD47 mAb reduces the proliferation of T lymphocytes. k . Blocking the interaction of CD47 on naïve T cells with TSP-1 prompts the generation of Tregs. l . The interaction between CD47 on B cell and SIRPα on macrophage and DC brings cell–cell interaction which is important to B cell maturation. m . CD19 and BCR co-transduce B cell signal to promote B cell activation and proliferation. The bispecific antibody targeting both CD19 and CD47 inhibits CD19 cluster to move to BCR and inhibits B cell proliferation finally.

Article Snippet: GeneScience , Gentulizumab , Monoclonal Antibody , CD47 , Solid Tumor/NHL , Phase 1 , , single-drug therapy , NCT05221385.

Techniques: Migration, Transformation Assay, Activation Assay, Expressing, Binding Assay, Transmigration Assay, Clinical Proteomics, Membrane, Transduction, Inhibition, Blocking Assay

 CD47-targeting  drugs in the clinical trial and investigational new drug (IND) stage (Please refer the separate excel).

Journal: Journal of Advanced Research

Article Title: Deciphering the role of CD47 in cancer immunotherapy

doi: 10.1016/j.jare.2023.10.009

Figure Lengend Snippet: CD47-targeting drugs in the clinical trial and investigational new drug (IND) stage (Please refer the separate excel).

Article Snippet: GeneScience , Gentulizumab , Monoclonal Antibody , CD47 , Solid Tumor/NHL , Phase 1 , , single-drug therapy , NCT05221385.

Techniques:

 CD47  agonists in pre-clinical stage.

Journal: Journal of Advanced Research

Article Title: Deciphering the role of CD47 in cancer immunotherapy

doi: 10.1016/j.jare.2023.10.009

Figure Lengend Snippet: CD47 agonists in pre-clinical stage.

Article Snippet: GeneScience , Gentulizumab , Monoclonal Antibody , CD47 , Solid Tumor/NHL , Phase 1 , , single-drug therapy , NCT05221385.

Techniques: Activity Assay, Binding Assay, Blocking Assay, Derivative Assay