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* Respiratory Medicine Unit, Section of Functional Genomics, Division of Genomic Medicine, University of Sheffield, Royal Hallamshire Hospital, Sheffield, United Kingdom; and
Respiratory Medicine Division, Department of Medicine, University of Cambridge School of Medicine, Addenbrooke’s and Papworth Hospitals, Cambridge, United Kingdom
Neutrophil granulocytes have a short lifespan, with their survival
limited by a constitutive program of apoptosis. Acceleration of
neutrophil apoptosis following ligation of the Fas death receptor is
well-documented and TNF-
also has a transient proapoptotic effect.
We have studied the role of the death receptor ligand TRAIL in human
neutrophils. We identified the presence of mRNAs for TRAIL, TRAIL-R2,
and TRAIL-R3, and cell surface expression of TRAIL-R2 and -R3 in
neutrophil populations. Neutrophil apoptosis is specifically
accelerated by exposure to a leucine zipper-tagged form of TRAIL, which
mimics cell surface TRAIL. Using blocking Abs to TRAIL receptors,
specifically TRAIL-R2, and a TRAIL-R1:FcR fusion protein, we have
excluded a role for TRAIL in regulating constitutive neutrophil
apoptosis. No additional proapoptotic effect of leucine zipper TRAIL
was identified following TRAIL treatment of neutrophils in the presence
of gliotoxin, an inhibitor of NF-
B, suggesting TRAIL does not
activate NF-B in human neutrophils. TRAIL treatment of human
neutrophils did not induce a chemotactic response. The susceptibility
of neutrophils to TRAIL-mediated apoptosis suggests a role for TRAIL in
the regulation of inflammation and may provide a mechanism for
clearance of neutrophils from sites of
inflammation.
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