S100A9 promotes the activation of proinflammatory pathways in primary B-CLL cells from patients with progressive disease. CLL PBMCs were incubated with and without rhS100A9 for 72 hours, and several parameters were assessed. (A-C) Phosphorylation levels of AKT1 (Ser473 and Thr308), IKK (Ser176/180), and JNK (Thr183/185) were measured in CD19+CD5+ cells by FC. (D) JUN and FOS mRNA expression was assessed by qPCR. (E) Expression of the antiapoptotic proteins MCL-1 and BCL-2 in CD19+CD5+ was also evaluated by FC. (F) A multiplex cytokine assay was performed in PBMCs from patients with CLL after S100A9 in vitro stimulation for 24 hours. ∗∗∗∗P < .0001; ∗∗∗P < .001; ∗∗P < .005; ∗P < .05 (paired t test). Ctrl, Control of unstimulated cells; MCL-1, myeloid cell leukemia-1; MFI, median fluorescence intensity; ns, not significant.
Figure 1.

S100A9 promotes the activation of proinflammatory pathways in primary B-CLL cells from patients with progressive disease. CLL PBMCs were incubated with and without rhS100A9 for 72 hours, and several parameters were assessed. (A-C) Phosphorylation levels of AKT1 (Ser473 and Thr308), IKK (Ser176/180), and JNK (Thr183/185) were measured in CD19+CD5+ cells by FC. (D) JUN and FOS mRNA expression was assessed by qPCR. (E) Expression of the antiapoptotic proteins MCL-1 and BCL-2 in CD19+CD5+ was also evaluated by FC. (F) A multiplex cytokine assay was performed in PBMCs from patients with CLL after S100A9 in vitro stimulation for 24 hours. ∗∗∗∗P < .0001; ∗∗∗P < .001; ∗∗P < .005; ∗P < .05 (paired t test). Ctrl, Control of unstimulated cells; MCL-1, myeloid cell leukemia-1; MFI, median fluorescence intensity; ns, not significant.

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