Fig. 4.
Fig. 4. CEM-C7H2 T-ALL cells are eliminated by myeloma cells via the Fas/FasL pathway. CEM-C7H2 T-ALL cells were labeled with 3[H]-thymidine for 5 hours and cocultivated with the indicated neoplastic plasma cell lines, respectively, for 72 hours. An efficient, predetermined E/T ratio of 10:1 was applied. The decrease in DNA-incorporated radioactivity was used to calculate the degree of cell death induced in target T cells by their cocultivation with malignant plasma cells (▪). Treatment of T cells with 0.25 μg/mL of the agonistic anti-Fas MoAb served as an internal control of the assay. Blockage of the Fas receptor with the antagonistic ZB4 anti-Fas MoAb (0.25 μg/mL, a) or neutralization of FasL molecules using the NOK-2 FasL MoAb (2.5 μg/mL, b) was performed to prove the dependence of the observed cytotoxicity on active Fas signaling (□). Mean values ± SEM (n = 8) are depicted.

CEM-C7H2 T-ALL cells are eliminated by myeloma cells via the Fas/FasL pathway. CEM-C7H2 T-ALL cells were labeled with 3[H]-thymidine for 5 hours and cocultivated with the indicated neoplastic plasma cell lines, respectively, for 72 hours. An efficient, predetermined E/T ratio of 10:1 was applied. The decrease in DNA-incorporated radioactivity was used to calculate the degree of cell death induced in target T cells by their cocultivation with malignant plasma cells (▪). Treatment of T cells with 0.25 μg/mL of the agonistic anti-Fas MoAb served as an internal control of the assay. Blockage of the Fas receptor with the antagonistic ZB4 anti-Fas MoAb (0.25 μg/mL, a) or neutralization of FasL molecules using the NOK-2 FasL MoAb (2.5 μg/mL, b) was performed to prove the dependence of the observed cytotoxicity on active Fas signaling (□). Mean values ± SEM (n = 8) are depicted.

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