Fig. 7.
Fig. 7. Killing of primary B-CLL cells by chimeric HLA class II antibodies. / Chimeric IgG1, IgA1, or IgA2 versions of HLA class II antibody F3.3 were compared in ADCC against 51Cr-labeled, freshly isolated B-CLL cells. As effector source, we used unseparated blood from healthy donors or from G-CSF–primed patients (G-CSF). Both donor groups mediated significant killing (indicated by *) with all 3 antibody isotypes. Notably, only IgA1- and IgA2-mediated lysis, not IgG1-mediated lysis, was significantly enhanced during G-CSF therapy. Killing without antibody or without effectors was consistently low. Data are presented as mean percentage specific lysis ± SEM from experiments with at least 4 different donors from each group. Significant (P < .05) differences between healthy donors and G-CSF–primed patients are indicated by #.

Killing of primary B-CLL cells by chimeric HLA class II antibodies.

Chimeric IgG1, IgA1, or IgA2 versions of HLA class II antibody F3.3 were compared in ADCC against 51Cr-labeled, freshly isolated B-CLL cells. As effector source, we used unseparated blood from healthy donors or from G-CSF–primed patients (G-CSF). Both donor groups mediated significant killing (indicated by *) with all 3 antibody isotypes. Notably, only IgA1- and IgA2-mediated lysis, not IgG1-mediated lysis, was significantly enhanced during G-CSF therapy. Killing without antibody or without effectors was consistently low. Data are presented as mean percentage specific lysis ± SEM from experiments with at least 4 different donors from each group. Significant (P < .05) differences between healthy donors and G-CSF–primed patients are indicated by #.

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