Figure 1.
Blockade of CD47-SIRPα interactions improves CD20 IgG1 antibody–mediated ADCP by macrophages but does not trigger ADCC by PMNs. Macrophage-mediated ADCP was assessed by fluorescence microscopy (A), whereas ADCC by PMNs was investigated in 3-hour [51Cr] release assays (B). An IgG2σ version of the CD47 antibody 5F9 (10 µg/mL) was used to block CD47-SIRPα interactions. Mino (mantle cell lymphoma) and Raji (Burkitt lymphoma) cells served as target cells (left and right panels, respectively). The CD20 antibody RTX, OFA, or OBI was used at 10 µg/mL; E:T ratios were 80:1 in ADCC assays and 1:2 in ADCP assays. Results are mean ± SEM from ≥3 experiments with effector cells from different donors. *Significant ADCP by CD20 antibodies vs control (ctrl.) antibody. XSignificant differences in the absence or presence of CD47 blockade. Significant differences (P < .05) were calculated using ANOVA. n.s., not significant; PI, phagocytic index.

Blockade of CD47-SIRPα interactions improves CD20 IgG1 antibody–mediated ADCP by macrophages but does not trigger ADCC by PMNs. Macrophage-mediated ADCP was assessed by fluorescence microscopy (A), whereas ADCC by PMNs was investigated in 3-hour [51Cr] release assays (B). An IgG2σ version of the CD47 antibody 5F9 (10 µg/mL) was used to block CD47-SIRPα interactions. Mino (mantle cell lymphoma) and Raji (Burkitt lymphoma) cells served as target cells (left and right panels, respectively). The CD20 antibody RTX, OFA, or OBI was used at 10 µg/mL; E:T ratios were 80:1 in ADCC assays and 1:2 in ADCP assays. Results are mean ± SEM from ≥3 experiments with effector cells from different donors. *Significant ADCP by CD20 antibodies vs control (ctrl.) antibody. XSignificant differences in the absence or presence of CD47 blockade. Significant differences (P < .05) were calculated using ANOVA. n.s., not significant; PI, phagocytic index.

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