![Fig. 5. In K562 cells, apoptosis is induced, which is distinct from the interaction of FasL/Fas, TNF-/TNFR, and IL-8/IL-8R. (A and B) After 2 hours of preincubation with 1 μg of anti-Fas MoAb (IgG2b, clone SM1/23) or 1 μg of anti-TNFR(p55) MoAb (IgG), K562 cells (A) and CCRF-CEM cells (B) at a concentration of 1 × 105cells/mL were exposed to 10 μg/mL β2m or at 37°C for 48 hours. β2m-induced apoptosis in both cell lines were prevented by neither anti-Fas MoAb nor anti-TNFR MoAb. (C and D) The preincubations with each 5 μg/mL of anti–IL-8 MoAb and anti–IL-8 receptor antibodies (receptor A [RA] and receptor B [RB]) did not inhibit the induction of apoptosis in K562 cells (C) and in CCRF-CEM cells (D) as described above. In addition, 10 ng/mL of anti-Fas MoAb, 10 ng/mL of recombinant human TNF-, and 20 ng/mL of endothelial IL-8 (data not shown) were used as apoptosis-inducing factors in control studies. Apoptotic cells were assayed by TUNEL. Data are expressed as the mean ± SE of 3 independent experiments.](https://ash.silverchair-cdn.com/ash/content_public/journal/blood/94/8/10.1182_blood.v94.8.2744.420k34_2744_2753/7/blod42034005x.jpeg?Expires=1735818493&Signature=UBEkbistRJvt2JRGN~0ksaI2hTWmXN1geybH8WrUKzSR0ZIjiImPt7kdrqlzY5ug5vjSXDozK0OxC7-AhfKPEuTmy--teBfcDWcrQL~wSTBt9vjLRm1xSbbAP9BTlAQU8cSvat6wy9xG6yqWzObuTo3WEhKgSlLYTGEzMAyIhgXOqflV~OFX6r6DJ7olhroiNhj1e0WJsgPe~VMDCQno5anC4yNeGaxnNzrvJe~XITqmfevftSt099YnuX5hMnJjU9JEySWm6hTBBoekZt3hTaxx3bEpvbWFCOmc~w-H3wWO9-jH0EN1D40GkXF9cooOtSQ8Oy0dgUIV2xp81XVwmw__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA)
In K562 cells, apoptosis is induced, which is distinct from the interaction of FasL/Fas, TNF-/TNFR, and IL-8/IL-8R. (A and B) After 2 hours of preincubation with 1 μg of anti-Fas MoAb (IgG2b, clone SM1/23) or 1 μg of anti-TNFR(p55) MoAb (IgG), K562 cells (A) and CCRF-CEM cells (B) at a concentration of 1 × 105cells/mL were exposed to 10 μg/mL β2m or at 37°C for 48 hours. β2m-induced apoptosis in both cell lines were prevented by neither anti-Fas MoAb nor anti-TNFR MoAb. (C and D) The preincubations with each 5 μg/mL of anti–IL-8 MoAb and anti–IL-8 receptor antibodies (receptor A [RA] and receptor B [RB]) did not inhibit the induction of apoptosis in K562 cells (C) and in CCRF-CEM cells (D) as described above. In addition, 10 ng/mL of anti-Fas MoAb, 10 ng/mL of recombinant human TNF-, and 20 ng/mL of endothelial IL-8 (data not shown) were used as apoptosis-inducing factors in control studies. Apoptotic cells were assayed by TUNEL. Data are expressed as the mean ± SE of 3 independent experiments.
