Figure 2
Figure 2. ADCC of type I and II antibodies. (A) Transgenic hCD20 murine B cells were loaded with Calcein-AM and opsonized with anti-CD20 mAbs (N = 3). B cells were then cocultured with mNK cells for 2 hours at an E:T ratio of 10:1; supernatant was assayed for calcein release at 490 nm. (B) Levels of ADCC when target hCD20 murine B cells were opsonized with 10 µg/mL mAbs and cocultured with mNK cells. Statistical analyses were carried out using 1-way ANOVA with multiple comparisons and significance was accepted at *P < .05, **P < .01, and ***P < .001. (C) Primary human CLL cells were loaded with Calcein-AM and opsonized with 0.001 to 10 µg/mL anti-CD20 mAbs (N = 2). CLL cells were then cocultured with human peripheral blood mononuclear cells for 4 hours at an E:T ratio of 50:1; supernatant was assayed for calcein release at 490 nm.

ADCC of type I and II antibodies. (A) Transgenic hCD20 murine B cells were loaded with Calcein-AM and opsonized with anti-CD20 mAbs (N = 3). B cells were then cocultured with mNK cells for 2 hours at an E:T ratio of 10:1; supernatant was assayed for calcein release at 490 nm. (B) Levels of ADCC when target hCD20 murine B cells were opsonized with 10 µg/mL mAbs and cocultured with mNK cells. Statistical analyses were carried out using 1-way ANOVA with multiple comparisons and significance was accepted at *P < .05, **P < .01, and ***P < .001. (C) Primary human CLL cells were loaded with Calcein-AM and opsonized with 0.001 to 10 µg/mL anti-CD20 mAbs (N = 2). CLL cells were then cocultured with human peripheral blood mononuclear cells for 4 hours at an E:T ratio of 50:1; supernatant was assayed for calcein release at 490 nm.

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