Fig. 4.
Fig. 4. (A) Defective Fas-mediated apoptosis of patients' lymphocytes (○, M.F.; □, N.F.; ▵, S.F.) as compared with normal induction of apoptosis on lymphocytes from parents (•, father; ▪, mother) and five healthy controls (▴). Cells were activated with PHA (1.2 μg/mL) for 2 days and IL-2 (20 U/mL) for 5 days and then incubated for 24 hours with or without various concentrations of an anti-Fas antibody known to deliver an apoptotic signal (CH11). The percentage of apoptotic cells as a function of the CH11 antibody concentration is shown. For healthy controls, data are expressed as mean ± 1 SD. One representative experiment of three is shown. (B) Normal dexamethasone-induced apoptosis of lymphocytes from all affected siblings as compared with their parents and three healthy controls. Cells were activated with PHA (1.2 μg/mL) for 2 days and IL-2 (20 U/mL) for 5 days and then incubated for 24 hours with or without dexamethasone 10-5 mol/L. The percentage of apoptotic cells is shown.

(A) Defective Fas-mediated apoptosis of patients' lymphocytes (○, M.F.; □, N.F.; ▵, S.F.) as compared with normal induction of apoptosis on lymphocytes from parents (•, father; ▪, mother) and five healthy controls (▴). Cells were activated with PHA (1.2 μg/mL) for 2 days and IL-2 (20 U/mL) for 5 days and then incubated for 24 hours with or without various concentrations of an anti-Fas antibody known to deliver an apoptotic signal (CH11). The percentage of apoptotic cells as a function of the CH11 antibody concentration is shown. For healthy controls, data are expressed as mean ± 1 SD. One representative experiment of three is shown. (B) Normal dexamethasone-induced apoptosis of lymphocytes from all affected siblings as compared with their parents and three healthy controls. Cells were activated with PHA (1.2 μg/mL) for 2 days and IL-2 (20 U/mL) for 5 days and then incubated for 24 hours with or without dexamethasone 10-5 mol/L. The percentage of apoptotic cells is shown.

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