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. Author manuscript; available in PMC: 2020 Feb 17.
Published in final edited form as: Nat Med. 2019 Mar 4;25(4):612–619. doi: 10.1038/s41591-019-0356-z

Extended Figure 6. Synergy between blockade of CD47 pyroglutamate formation and tumors opsonization in tumor cell killing by macrophages and neutrophils.

Extended Figure 6

a, MFI of lamin B-Turquoise of the total CD11b+ macrophage population in samples incubated with control (DMSO)-treated (-) or SEN177-treated (+) Turquoise-expressing Burkitt’s lymphoma (Raji) cells in the presence or absence of the anti-human CD20 antibody Rituximab, CD47-blocking F(ab’)2 fragment B6H12, or SIRPα blocking antibody 12C4, as determined by ImageStream analysis. Symbols represent individual donors. Data represent mean ± s.d. of independent donors. ***P<0.0001; **P=0.0016; *P=0.0256 by one-way ANOVA with multiple comparison correction. b, Specific lysis of control (DMSO)-treated (-) or SEN177-treated (+) WT, QPCTL KO or CD47 KO epidermoid carcinoma (A431) cells by human neutrophils in the presence or absence of the anti-human EGFR antibody cetuximab in a 4 hour 51Cr-release assay. Data represent mean ± s.d. of independent donors. ***P<0.0001; 0.0325≥*P≥0.0207 by one-way ANOVA with multiple comparison correction. n.s.; not significant. c, Flow cytometry plot of cell surface binding of anti-human CD20 antibody to Burkitt’s lymphoma (Raji) cells (left panel) and anti-human EGFR antibody to epidermoid carcinoma (A431) cells (right panel) treated with control (DMSO) or SEN177 for 4 days.

Data are representative of one (c) or at least three independent experiments (a, b) representing 4 donors (for B6H12(Fab’)2 conditions), 8 donors (all other conditions) (a), and 8 donors (b).