Figure 6
Figure 6. Autologous CML patient NK cells trigger CSL362-mediated ADCC against matching CD34+ cells. (A) CD34+ of CML patients, collected at the time of diagnosis, were incubated for 4 hours with NK cells, isolated from the same patients after achieving complete cytogenetic response (see Table 1), at an E:T of 10:1 in the absence and presence of CSL362, and remaining CFUs were enumerated (left panel). In parallel, CML CD34+ cells were subjected to healthy donor NK cell–induced CSL362-mediated ADCC (right panel). (B) Normal CD34+ cells were used as targets of CSL362-mediated ADCC conferred by either autologous or allogeneic NK cells. (C) The long-term culture-initiating potential of normal and CML LSPCs subjected to CSL362-dependent autologous NK cell–mediated cytotoxicity is evaluated. All data are normalized to target cells alone.

Autologous CML patient NK cells trigger CSL362-mediated ADCC against matching CD34+ cells. (A) CD34+ of CML patients, collected at the time of diagnosis, were incubated for 4 hours with NK cells, isolated from the same patients after achieving complete cytogenetic response (see Table 1), at an E:T of 10:1 in the absence and presence of CSL362, and remaining CFUs were enumerated (left panel). In parallel, CML CD34+ cells were subjected to healthy donor NK cell–induced CSL362-mediated ADCC (right panel). (B) Normal CD34+ cells were used as targets of CSL362-mediated ADCC conferred by either autologous or allogeneic NK cells. (C) The long-term culture-initiating potential of normal and CML LSPCs subjected to CSL362-dependent autologous NK cell–mediated cytotoxicity is evaluated. All data are normalized to target cells alone.

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