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. 2023 Aug 1;37(10):2036–2049. doi: 10.1038/s41375-023-01984-z

Fig. 6. Selinexor enhances NK cell activation against CLL cells in combination with acalabrutinib.

Fig. 6

Expression of HLA-E (A) and total HLA class I proteins (B) on CD19 + CD5 + CLL cells after treatment with selinexor (500 nM) and the BTK inhibitors Ibrutinib (Ibr, 1 µM) and Acalabrutinib (ACP, 1 µM) as indicated for 24 h. Shown is mean ± SEM (N = 5) and significant differences in ligand expression between treatments were calculated with repeated-measure one-way ANOVA followed by Tukey’s post-hoc test (*P < 0.05). C NK specific lysis of CLL targets pre-treated for 24 h with selinexor (500 nM), Ibr (1 µM) or ACP (1 µM) alone or in combination as indicated (E:T = 5:1). Shown is the mean ± SEM (N = 4) and differences in NK cell specific lysis between combination treatments were calculated with repeated-measure one-way ANOVA. D NK cell activation as measured by fold change in CD107a staining when healthy donor PBMC were co-cultured with CLL cells pre-treated for 24 h with selinexor (500 nM), Ibr (1 µM) and ACP (1 µM) as indicated (E:T = 5:1). During the 4-h co-culture, selinexor and BTK inhibitors were re-added to appropriate wells. Shown is the mean ± SEM (N = 12) and differences in NK cell activation between treatments were assessed by repeated-measure one-ANOVA followed by Tukey’s post-hoc test (*P < 0.05, ***P < 0.005, ****P < 0.001). ns nonsignificant.