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. 2018 Oct 12;9(80):35123–35140. doi: 10.18632/oncotarget.26212

Figure 4. BTK is activated by CXCL12 and mediates adhesion of CLL B-lymphocytes to ICAM-1 and VCAM-1.

Figure 4

(A) Cells were treated with buffer (NT) or CXCL12 for indicated times. Mean ± SD. *, P < 0.05, versus NT. Data are average of n = 4 independent experiments. (B) Cells were treated for 1 h with vehicle (NT and Control) or Ibrutinib 10 μM and stimulated with CXCL12 0.5 μM for 120 sec. Mean ± SD. **, P < 0.01, versus Control. Data are average of n = 4 independent experiments. (C) Histograms of fluorescence of a representative experiment of data shown in (A). (D) Histograms of fluorescence of a representative experiment of data shown in (B). Static adhesion to ICAM-1 (E) or VCAM-1 (F): cells were treated for 1 h with vehicle (Control) or the indicated doses of Ibrutinib, and stimulated with buffer (No) or CXCL12 0.5 μM for 120 sec. Mean ± SD. *, P < 0.01; **, P < 0.001, versus Control. Data are average of n = 20 independent experiments in duplicate. Under-flow adhesion to ICAM-1 (G) or VCAM-1 (H): cells were treated for 1 h with vehicle (Control) or with Ibrutinib 10 μM. Mean ± SD. *, P < 0.05, versus Control. Data are average of n = 3 independent experiments.