anti cd47 mab be0283  (Bio X Cell)

Journal: Leukemia

Article Title: Blocking the CD47-SIRPα interaction reverses the disease phenotype in a polycythemia vera mouse model

doi: 10.1038/s41375-023-01903-2

Figure Lengend Snippet: List of antibodies.

Article Snippet: Six days after biotin injection, mice were treated intraperitoneally 3 times a week for 2 weeks with an anti-mouse CD47 mAb (clone MIAP410; BioXCell) or a mouse IgG1 isotype control (clone MOPC-21; BioXCell) at a dose of 200 μg/mouse.

Techniques:

Journal: Leukemia

Article Title: Blocking the CD47-SIRPα interaction reverses the disease phenotype in a polycythemia vera mouse model

doi: 10.1038/s41375-023-01903-2

Figure Lengend Snippet: A Experimental workflow for the treatment of wild-type (WT) and JAK2 mutant (PV) mice with an anti-IgG1 control (IgG1) or an anti-CD47 antibody. One million ubiquitin-GFP ( UBC-GFP )-positive WT bone marrow (BM) cells were mixed with one million BM cells extracted from PV mice and transplanted into lethally irradiated WT recipients. Antibody treatment was performed 3 times a week for 2 or 4 weeks. Mice were sacrificed and analyzed after that. B Hemoglobin, platelet, and neutrophil counts (WT IgG1, n = 9; WT anti-CD47, n = 9; PV IgG1, n = 24; PV anti-CD47, n = 25) and ( C ) spleen weight (WT IgG1, n = 4; WT anti-CD47, n = 4; PV IgG1, n = 15; PV anti-CD47, n = 15) determined after 2 weeks of treatment. Gray shaded area indicates the normal range. D Blood counts and ( E ) spleen weight after 4 weeks of treatment. WT IgG1, n = 10; WT anti-CD47, n = 10; PV IgG1, n = 14; PV anti-CD47, n = 14. WT blue symbols, PV red symbols. Results are represented as mean ± standard deviation. ns not significant, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 (Kruskal–Wallis test with Dunn’s multiple comparisons for B (hemoglobin and platelet counts), C , D (platelet counts), and E ; two-way ANOVA with Tukey’s multiple comparisons test for B (neutrophil counts), and D (hemoglobin and neutrophil counts).

Article Snippet: Six days after biotin injection, mice were treated intraperitoneally 3 times a week for 2 weeks with an anti-mouse CD47 mAb (clone MIAP410; BioXCell) or a mouse IgG1 isotype control (clone MOPC-21; BioXCell) at a dose of 200 μg/mouse.

Techniques: Mutagenesis, Control, Ubiquitin Proteomics, Irradiation, Standard Deviation

Journal: Leukemia

Article Title: Blocking the CD47-SIRPα interaction reverses the disease phenotype in a polycythemia vera mouse model

doi: 10.1038/s41375-023-01903-2

Figure Lengend Snippet: A Gating strategy for the Lin-Sca-1 + c-Kit + (LSK) compartment and multipotent progenitors (MPPs), including long-term HSCs (HSC LT ), short-term HSCs (HSC ST ), MPP2, MPP3, and MPP4. PV IgG1, n = 15; PV anti-CD47, n = 15. B LSK fraction determined in the bone marrow (BM) and spleen (SPL). C Composition of the LSK compartment and MPPs in PV mice treated with IgG1 or anti-CD47 determined by flow cytometry at terminal analysis in the BM (top) and SPL (bottom). D Gating strategy for erythroid differentiation. Proerythroblasts (I; FSChi CD44hi), basophilic erythroblasts (II; FSCint CD44hi), polychromatic erythroblasts (III; FSCint CD44int), orthochromatic erythroblasts (IV; FSClo CD44int), and erythroblasts (V; FSClo CD44-). WT IgG1, n = 4; WT anti-CD47, n = 4; PV IgG1, n = 15; PV anti-CD47, n = 15. E Percentages of erythroid progenitors in the BM (left) and SPL (right) (% of FSC CD44 out of CD11b-CD45.2-Ter119+) determined by flow cytometry at terminal analysis. Results are represented as mean ± standard deviation. ns not significant, * p < 0.05 (Kruskal–Wallis test with Dunn’s multiple comparisons for B (BM LSK fraction); two-way ANOVA with Tukey’s multiple comparisons test for B (SPL LSK fraction); unpaired student’s t -test or Mann–Whitney test for C ).

Article Snippet: Six days after biotin injection, mice were treated intraperitoneally 3 times a week for 2 weeks with an anti-mouse CD47 mAb (clone MIAP410; BioXCell) or a mouse IgG1 isotype control (clone MOPC-21; BioXCell) at a dose of 200 μg/mouse.

Techniques: Flow Cytometry, Standard Deviation, MANN-WHITNEY

Journal: Leukemia

Article Title: Blocking the CD47-SIRPα interaction reverses the disease phenotype in a polycythemia vera mouse model

doi: 10.1038/s41375-023-01903-2

Figure Lengend Snippet: A UMAP with FlowSOM overlay of total live CD45.2 + Lin-Neutrophil-Eosinophil- cells. 18,000 cells of combined samples are shown per group. Wild-type (WT) and JAK2 mutant (PV) mice were treated with an anti-IgG1 control (IgG1) or an anti-CD47 antibody. WT IgG1, n = 3; WT anti-CD47, n = 3; PV IgG1, n = 3; PV anti-CD47, n = 4. B Bar plot depicting the total count of indicated FlowSOM-generated subpopulations per sample. Each bar represents one mouse. C The total count of FlowSOM-generated monocyte-derived effector cell (Mdc) population, shown per group. D Correlation of the hemoglobin change (treatment/baseline) to the Mdc cell number. E Antigen expression of indicated markers in FlowSOM-generated Mdc population, shown per group. The color and the circle size represent the mean of the median antigen expression of all samples per group. F Median expression and 25th and 75th percentiles of MerTK in FlowSOM-generated Mdc population. G Correlation of the hemoglobin change (treatment/baseline) to the medium expression of MerTK. WT, blue symbols; PV, red symbols. Results are represented as mean ± standard deviation. ns not significant, * p < 0.05, ** p < 0.01, *** p < 0.001 (two-way ANOVA with Tukey’s multiple comparisons test for C ; linear correlation and regression for D and G ; Brown–Forsythe and Welch one-way ANOVA followed by Dunnett T3 post-hoc test for F ).

Article Snippet: Six days after biotin injection, mice were treated intraperitoneally 3 times a week for 2 weeks with an anti-mouse CD47 mAb (clone MIAP410; BioXCell) or a mouse IgG1 isotype control (clone MOPC-21; BioXCell) at a dose of 200 μg/mouse.

Techniques: Mutagenesis, Control, Generated, Derivative Assay, Expressing, Standard Deviation

Journal: Leukemia

Article Title: Blocking the CD47-SIRPα interaction reverses the disease phenotype in a polycythemia vera mouse model

doi: 10.1038/s41375-023-01903-2

Figure Lengend Snippet: A Experimental workflow for the in vitro phagocytosis assay of wild-type (WT) and JAK2 mutant (PV) macrophages with WT or PV RBCs treated with an anti-IgG1 control (IgG1) or an anti-CD47 antibody. Created with BioRender.com. Percentage of labeled WT RBCs ( B ) and PV RBCs ( C ) out of F4/80+ spleen macrophages from WT and PV mice either treated with IgG1 or anti-CD47. Representative flow cytometry plots are shown on the left. D Percentage of labeled WT RBCs and JAK2 mutant RBCs (PV RBCs) out of WT (left) and PV (right) F4/80+ spleen macrophages either treated with IgG1 or anti-CD47. WT, blue symbols; PV, red symbols. Results are represented as mean ± standard deviation. ns not significant, * p < 0.05, ** p < 0.01, **** p < 0.0001 (two-way ANOVA with Tukey’s multiple comparisons test for B – D ).

Article Snippet: Six days after biotin injection, mice were treated intraperitoneally 3 times a week for 2 weeks with an anti-mouse CD47 mAb (clone MIAP410; BioXCell) or a mouse IgG1 isotype control (clone MOPC-21; BioXCell) at a dose of 200 μg/mouse.

Techniques: In Vitro, Phagocytosis Assay, Mutagenesis, Control, Labeling, Flow Cytometry, Standard Deviation