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1
*
Laboratory of Immunology, Institute of Hematologic Research, National Academy of Medicine, and
Department of Microbiology, Laboratory of Immunogenetics, Buenos Aires University School of Medicine, Buenos Aires, Argentina
We examined the ability of TNF-
to modulate human neutrophil
apoptosis. Neutrophils cultured with TNF- alone undergo a low but
significant increase in the number of apoptotic cells. More
interestingly, when neutrophils were pretreated with TNF- for 1–2
min at 37°C and then were exposed to a variety of agents such as
immobilized IgG, IgG-coated erythrocytes, complement-treated
erythrocytes, zymosan, PMA, zymosan-activated serum, fMLP,
Escherichia coli, and GM-CSF for 3 h at 37°C, a
marked stimulation of apoptosis was observed. Similar results were
obtained in neutrophils pretreated with TNF- for 30 min, 1 h,
3 h, and 18 h. Dose-dependent studies showed that TNF-
enhances neutrophil apoptosis at concentrations ranging from 1 to 100
ng/ml. In contrast to the observations made in neutrophils pretreated
with TNF-, there was no stimulation of apoptosis when TNF- was
added to neutrophils previously activated by conventional agonists.
Experiments performed to establish the mechanism through which TNF-
promotes neutrophil apoptosis showed that neither reactive oxygen
intermediates nor the Fas/Fas ligand system appear to be involved. Our
results suggest that TNF- plays a critical role in the control of
neutrophil survival by virtue of its ability to induce an apoptotic
death program which could be triggered by a variety of conventional
agonists.
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