TACI-Ig attenuates spontaneous as well as BAFF- and APRIL-induced survival and proliferation of malignant HRS cells. (A) Apoptosis and necrosis in HD-MyZ HRS cells incubated for 2 days in the presence or absence of control Ig, TACI-Ig, and BAFF-R–Ig. Early apoptotic, late apoptotic, and necrotic cells were annexin-V⁺propidium iodide^-, annexin-V⁺propidium iodide⁺, and annexin-V⁻propidium iodide⁺, respectively. Bars indicate SD of 4 experiments; *P < .05 and **P < .005 versus cells incubated with medium, respectively (leftmost bar of each cluster). (B) Proliferation of HD-MyZ HRS cells incubated for 2 days with or without BAFF and APRIL and in the presence or absence of control Ig, TACI-Ig, and BAFF-R–Ig. Bars indicate SD of 4 experiments; *P < .05 and **P < .005 versus cells incubated with medium, respectively (leftmost bar of each cluster). (C-D) Viability and proliferation of HD-MyZ HRS cells incubated for 2 days with or without a control, or anti-TACI or anti-BCMA antibody immobilized on CD32-L cells. Bars indicate SD of 4 experiments; *P < .05 and **P < .005 versus cells incubated with medium, respectively (leftmost bar of each panel). (E-F) Apoptosis, proliferation, and NF-κB–DNA binding activity of HD-MyZ HRS cells incubated for 2 days with control, BAFF, APRIL, TACI, and/or BCMA siRNAs. Bars indicate SD of 4 experiments; *P < .05, *P < .005, and **P < .001 versus cells incubated with control siRNA, respectively (leftmost bar of each panel). Antibodies to p65, p50, and c-Rel as well as a cold NF-κB–binding probe were used in supershift assays (bottom-right gel) to identify NF-κB–DNA complexes.