Figure 6.
WT1-TCB*–mediated cytotoxicity in combination with lenalidomide (Lena). (A) WT1-TCB–mediated specific lysis of primary AML cells significantly increased in combination with Lena after 4 days of coculture with HD T cells (n = 9-10). Lena was added at a concentration of 10 μM together with 10 nM WT1-TCB* in ex vivo cytotoxicity assays with primary AML cells and HD T cells at an E:T ratio of 1:2 for 4 days. (B) Levels of proinflammatory cytokines increase after combination of WT1-TCB* with Lena and levels of the anti-inflammatory interleukin 10 (IL-10) decrease (n = 9). (C) Representative example of CD45RA and CCR7 expression analysis. (D) Percentages of central memory T cells after 7 to 10 days of treatment (n = 8). Bars represent the mean ± SEM. Statistical analysis: Wilcoxon matched-pairs signed-rank test. *P < .05, **P < .01. n.s., not significant; TNF-α, tumor necrosis factor α.

WT1-TCB*–mediated cytotoxicity in combination with lenalidomide (Lena). (A) WT1-TCB–mediated specific lysis of primary AML cells significantly increased in combination with Lena after 4 days of coculture with HD T cells (n = 9-10). Lena was added at a concentration of 10 μM together with 10 nM WT1-TCB* in ex vivo cytotoxicity assays with primary AML cells and HD T cells at an E:T ratio of 1:2 for 4 days. (B) Levels of proinflammatory cytokines increase after combination of WT1-TCB* with Lena and levels of the anti-inflammatory interleukin 10 (IL-10) decrease (n = 9). (C) Representative example of CD45RA and CCR7 expression analysis. (D) Percentages of central memory T cells after 7 to 10 days of treatment (n = 8). Bars represent the mean ± SEM. Statistical analysis: Wilcoxon matched-pairs signed-rank test. *P < .05, **P < .01. n.s., not significant; TNF-α, tumor necrosis factor α.

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