EMMPRIN blocking prevents S100A9-mediated activation of proinflammatory pathways. (A-C) Expression levels of S100A9 receptors TLR4, RAGE, and EMMPRIN were compared between B cells from HDs and CD19+CD5+ cells from thawed PBMCs using FC. (D-G) CLL PBMCs were stimulated with rhS100A9 and treated with S100A9 inhibitors (TasQ [10 μM] or PaQ [10 μM]) or EMMPRIN-blocking antibody [10 μg/mL] for 72 hours. Phospho-AKT1(Ser473 and Thr308), phospo-IKK(Ser176/180), and phospo-JNK(Thr183/185) were assessed in CD19+CD5+ cells by FC. Cells without rhS100A9 stimulation were used as control. ∗∗∗∗P < .0001; ∗∗∗P < .001; ∗∗P < .005; ∗P < .05 (panels A-C, unpaired t test; panels D-G, 1-way analysis of variance). Ctrl, Control of unstimulated cells; HD, healthy donor; MFI, median fluorescence intensity; ns, not significant.
Figure 2.

EMMPRIN blocking prevents S100A9-mediated activation of proinflammatory pathways. (A-C) Expression levels of S100A9 receptors TLR4, RAGE, and EMMPRIN were compared between B cells from HDs and CD19+CD5+ cells from thawed PBMCs using FC. (D-G) CLL PBMCs were stimulated with rhS100A9 and treated with S100A9 inhibitors (TasQ [10 μM] or PaQ [10 μM]) or EMMPRIN-blocking antibody [10 μg/mL] for 72 hours. Phospho-AKT1(Ser473 and Thr308), phospo-IKK(Ser176/180), and phospo-JNK(Thr183/185) were assessed in CD19+CD5+ cells by FC. Cells without rhS100A9 stimulation were used as control. ∗∗∗∗P < .0001; ∗∗∗P < .001; ∗∗P < .005; ∗P < .05 (panels A-C, unpaired t test; panels D-G, 1-way analysis of variance). Ctrl, Control of unstimulated cells; HD, healthy donor; MFI, median fluorescence intensity; ns, not significant.

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