Fig. 1.
Fig. 1. Preactivated PBMCs induce apoptosis in ECs. Quantitative microscopic analysis of DAPI-stained ECs after 48 hours of coculture. Cells were microscopically analyzed by counting apoptotic and nonapoptotic cells (n = 10 microscopic fields including an average of 70 cells per field). (A) PBMCs were either untreated (PBMC), irradiated (PBMC-IR; 4 Gy), or incubated with bacterial endotoxin (PBMC-LPS; 10 ng/mL) for 4 hours. (B) Human IL-10 (0.1 μg/mL) and MAK 195 (anti-TNF-α MoAb; 20 μg/mL) inhibit the apoptosis-inducing effects of either irradiated or LPS-treated PBMCs on ECs. Results are given as the percentage of apoptotic cells (± standard deviation [SD]). These results are representatives of at least four independent experiments. *,**P < .001 of apoptosis of control ECs versus ECs coincubated with preactivated PBMCs and control ECs versus ECs cocultured with preactivated PBMCs in the presence of IL-10 or anti–TNF-α MoAb MAK195.

Preactivated PBMCs induce apoptosis in ECs. Quantitative microscopic analysis of DAPI-stained ECs after 48 hours of coculture. Cells were microscopically analyzed by counting apoptotic and nonapoptotic cells (n = 10 microscopic fields including an average of 70 cells per field). (A) PBMCs were either untreated (PBMC), irradiated (PBMC-IR; 4 Gy), or incubated with bacterial endotoxin (PBMC-LPS; 10 ng/mL) for 4 hours. (B) Human IL-10 (0.1 μg/mL) and MAK 195 (anti-TNF-α MoAb; 20 μg/mL) inhibit the apoptosis-inducing effects of either irradiated or LPS-treated PBMCs on ECs. Results are given as the percentage of apoptotic cells (± standard deviation [SD]). These results are representatives of at least four independent experiments. *,**P < .001 of apoptosis of control ECs versus ECs coincubated with preactivated PBMCs and control ECs versus ECs cocultured with preactivated PBMCs in the presence of IL-10 or anti–TNF-α MoAb MAK195.

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