Figure 3.
Figure 3. IL-6 does not modulate HGS-ETR1 killing of HMCLs. (A) IL-6 starvation of IL-6–dependent HMCLs does not enhance HGS-ETR1 killing. IL-6–dependent HMCLs ANBL-6 and XG2 (125 000 cells/0.25 mL in a 96-well plate) were treated for 48 hours with increasing concentrations of HGS-ETR1 or HGS-ETR2 mAbs in the presence or absence of 3 ng/mL IL-6. The proportion of dead cells was determined as described in “Materials and methods.” (B) Adding IL-6 to IL-6–independent HMCLs did not prevent HGS-ETR1 killing. IL-6–independent HMCL KMS12PE and RPMI-8226 (125 000 cells/0.25 mL in a 96-well plate) were treated for 48 hours with increasing concentrations of HGS-ETR1 or HGS-ETR2 mAb in the presence or absence of 3 ng/mL IL-6.

IL-6 does not modulate HGS-ETR1 killing of HMCLs. (A) IL-6 starvation of IL-6–dependent HMCLs does not enhance HGS-ETR1 killing. IL-6–dependent HMCLs ANBL-6 and XG2 (125 000 cells/0.25 mL in a 96-well plate) were treated for 48 hours with increasing concentrations of HGS-ETR1 or HGS-ETR2 mAbs in the presence or absence of 3 ng/mL IL-6. The proportion of dead cells was determined as described in “Materials and methods.” (B) Adding IL-6 to IL-6–independent HMCLs did not prevent HGS-ETR1 killing. IL-6–independent HMCL KMS12PE and RPMI-8226 (125 000 cells/0.25 mL in a 96-well plate) were treated for 48 hours with increasing concentrations of HGS-ETR1 or HGS-ETR2 mAb in the presence or absence of 3 ng/mL IL-6.

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