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J Immunol ; 166(5): 3476-83, 2001 Mar 01.
Article in English | MEDLINE | ID: mdl-11207306

ABSTRACT

We examined the ability of TNF-alpha to modulate human neutrophil apoptosis. Neutrophils cultured with TNF-alpha alone undergo a low but significant increase in the number of apoptotic cells. More interestingly, when neutrophils were pretreated with TNF-alpha for 1-2 min at 37 degrees 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 degrees C, a marked stimulation of apoptosis was observed. Similar results were obtained in neutrophils pretreated with TNF-alpha for 30 min, 1 h, 3 h, and 18 h. Dose-dependent studies showed that TNF-alpha enhances neutrophil apoptosis at concentrations ranging from 1 to 100 ng/ml. In contrast to the observations made in neutrophils pretreated with TNF-alpha, there was no stimulation of apoptosis when TNF-alpha was added to neutrophils previously activated by conventional agonists. Experiments performed to establish the mechanism through which TNF-alpha promotes neutrophil apoptosis showed that neither reactive oxygen intermediates nor the Fas/Fas ligand system appear to be involved. Our results suggest that TNF-alpha 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.


Subject(s)
Apoptosis/immunology , Neutrophils/cytology , Neutrophils/immunology , Tumor Necrosis Factor-alpha/physiology , Annexin A5/metabolism , Blood/immunology , Cell Membrane/immunology , Cell Membrane/metabolism , Cell Survival/immunology , Cells, Cultured , Culture Media, Conditioned , Cytokines/physiology , Dose-Response Relationship, Immunologic , Fas Ligand Protein , Humans , Interphase/immunology , Ligands , Membrane Glycoproteins/physiology , Neutrophils/metabolism , Phosphatidylserines/metabolism , Protein Binding/immunology , Reactive Oxygen Species/metabolism , fas Receptor/physiology
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