IVIg accelerates spontaneous neutrophil death, which is enhanced after priming with GM-CSF or IFN-γ. Cell death was assessed by ethidium bromide uptake and flow cytometric analysis. (A) Acceleration of neutrophil death by treatment with IVIg or F(ab′)2 fragments of IVIg. IVIg effects were also determined in the presence of mAb F(ab′)2 fragments to block Fcγ receptors. Results of 24-hour cultures are shown (n = 4). **P < .01. ***P < .001. No statistical difference was seen between the different IVIg stimulation conditions. (B) Concentration-effect curve of IVIg in 20-hour neutrophil cultures. Maximal death effects in the absence of cytokine priming were seen at 20 mg/mL. GM-CSF, at low concentrations of IVIg, protected cells from spontaneous apoptosis, whereas it promoted death at higher concentrations (n = 3). (C) GM-CSF and IFN-γ, but not G-CSF, were able to enhance IVIg-mediated neutrophil death. Results of 24-hour cultures are shown (n = 4). **P < .01; ***P < .001.
