Fig. 2.
Fig. 2. (A) Induction of apoptosis in CD4+ and CD8+ cells from B-CLL patients (n = 30). PBMC from 30 B-CLL patients were cocultured with the agonistic anti-FasR MoAb CH11 (□) and/or the antagonistic anti-FasR MoAb ZB4 (▨) for 24 hours (up to 7 days, data not shown) in the indicated concentrations. The percentage of apoptosis in the relevant T-cell subpopulations was measured by two-color flow cytometry after staining with PE-conjugated anti-CD4 or anti-CD8 MoAb and AnnexinV-FITC and is shown in a box-blot and whiskers model. Statistical analysis showed the following relationships: CD4+ cells: untreated versus 100 ng CH11-treated (P = .0002), 100 ng CH11- versus 250 ng CH11-treated (P = .02), 250 ng CH11-treated versus 250 ng CH11+ZB4-treated (P < .002); CD8+ cells: untreated versus 250 ng CH11-treated (P > .2), 250 ng CH11-treated versus 250 ng CH11+ZB4-treated (P > .2). (B) Induction of apoptosis in CD4+ and CD8+cells from healthy donors (n = 20). PBMC from healthy volunteers were untreated or cocultured with the agonistic anti-FasR MoAb CH11 (□) and/or the antagonistic anti-FasR MoAb ZB4 (▨) for 24 hours (up to 7 days, data not shown). The percentage of apoptotic cells in CD4+ and CD8+ cell fractions were assessed by two-color flow cytometry as described for (A). Statistical analysis showed the following: CD4+ cells: untreated versus CH11 treated (P > .7), CH11-treated versus CH11+ZB4-treated (P > .8); CD8+ cells: untreated versus CH11 treated (P > .7), CH11-treated versus CH11+ZB4-treated (P > .3).

(A) Induction of apoptosis in CD4+ and CD8+ cells from B-CLL patients (n = 30). PBMC from 30 B-CLL patients were cocultured with the agonistic anti-FasR MoAb CH11 (□) and/or the antagonistic anti-FasR MoAb ZB4 (▨) for 24 hours (up to 7 days, data not shown) in the indicated concentrations. The percentage of apoptosis in the relevant T-cell subpopulations was measured by two-color flow cytometry after staining with PE-conjugated anti-CD4 or anti-CD8 MoAb and AnnexinV-FITC and is shown in a box-blot and whiskers model. Statistical analysis showed the following relationships: CD4+ cells: untreated versus 100 ng CH11-treated (P = .0002), 100 ng CH11- versus 250 ng CH11-treated (P = .02), 250 ng CH11-treated versus 250 ng CH11+ZB4-treated (P < .002); CD8+ cells: untreated versus 250 ng CH11-treated (P > .2), 250 ng CH11-treated versus 250 ng CH11+ZB4-treated (P > .2). (B) Induction of apoptosis in CD4+ and CD8+cells from healthy donors (n = 20). PBMC from healthy volunteers were untreated or cocultured with the agonistic anti-FasR MoAb CH11 (□) and/or the antagonistic anti-FasR MoAb ZB4 (▨) for 24 hours (up to 7 days, data not shown). The percentage of apoptotic cells in CD4+ and CD8+ cell fractions were assessed by two-color flow cytometry as described for (A). Statistical analysis showed the following: CD4+ cells: untreated versus CH11 treated (P > .7), CH11-treated versus CH11+ZB4-treated (P > .8); CD8+ cells: untreated versus CH11 treated (P > .7), CH11-treated versus CH11+ZB4-treated (P > .3).

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