FIGURE 5.

Natural killer (NK) cells enhance benralizumab-mediated macrophage (Mac) phagocytosis and cytotoxicity. Human macrophages were derived from peripheral blood monocytes after 7 days stimulation with 50 ng·mL⁻¹ macrophage colony-stimulating factor. Primary NK cells and eosinophils (Eos) were isolated from autologous healthy donors. Eosinophils were pre-treated with 10 nM of indicated antibodies. Cells were mixed for 6 h and analysed by flow cytometry. Supernatants were collected for quantification of tumour necrosis factor (TNF) by ELISA. a, b) Changes in macrophage markers involved in target recognition/internalisation (CD163, CD64 and signal regulatory protein α/β (SIRPα/β)) and phagolysosome activation (CD107a), represented as percentage of total CD163⁺ CD11b⁺ macrophages (n=5). c) TNF amounts quantified by ELISA post-treatment by benralizumab in the presence and absence of macrophages and NK cells (n=4). d) Quantification of TNF expression in macrophages in the presence and absence of NK cells represented as percentage of total CD163⁺ CD11b⁺ macrophages (n=4). b, c, d) Data are mean±sem. Two-way ANOVA test with Tukey's multiple comparisons. *: p<0.05; **: p<0.01; ***: p<0.001, benralizumab versus controls (isotype or parent fucosylated anti-interleukin-5 receptor α (PF anti-IL-5Rα)). ⁺: p<0.05; ⁺⁺: p<0.01, Eos+Mac+NK versus Eos+Mac. Statistical values are presented in supplementary table S2.