Inhibition of NF-κB activity in APLA/anti-β₂GPI–treated HUVECs by KLF2 or KLF4 is in part the result of CBP/p300. Endothelial cells were transfected with scrambled DNA (Scr DNA, control), or KLF2 or KLF4, in the absence or presence of siRNA to CBP/p300. All cells were also transfected with an NF-κB–luciferase reporter and Renilla luciferase. Cells were subsequently incubated with either medium alone, β₂GPI (100nM), and anti–human β₂GPI antibodies (600nM), or TNF (10 ng/mL) for 5 hours, then lysed before determination of NF-κB–dependent luciferase activity. KLF2 and KLF4 expression, in the absence of siCBP/p300, inhibited NF-κB transcriptional activation in the presence of β₂GPI and anti-β₂GPI antibodies compared with cells transfected with the control vector (*P < .008). siCBP/p300 inhibited NF-κB transcriptional activity independently, as well as in the presence of KLF2 or KLF4 (*P < .008). However, siCBP/p300 did not significantly affect NF-κB transcriptional activity in the presence of TNF-α. Error bars represent the mean ± SEM of quadruplicate points and data are representative of 3 independent experiments.