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Inflammatory neutrophils retain susceptibility to apoptosis mediated via the Fas death receptor
Author(s) -
Renshaw Stephen A.,
Timmons Samantha J.,
Eaton Vanessa,
Usher Lynne R.,
Akil Mohammed,
Bingle Colin D.,
Whyte Moira K. B.
Publication year - 2000
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.67.5.662
Subject(s) - apoptosis , inflammation , immunology , biology , granulocyte , fas ligand , receptor , programmed cell death , fas receptor , macrophage , rheumatoid arthritis , in vitro , biochemistry
Apoptosis and clearance of neutrophils is essential for successful resolution of inflammation. Altered signaling via the Fas receptor could explain the observed prolongation of neutrophil lifespan and associated tissue injury at inflammatory sites. We therefore compared inflammatory neutrophils extracted from joints of rheumatoid arthritis patients, with peripheral blood neutrophils. Inflammatory neutrophils underwent constitutive apoptosis in culture more rapidly than peripheral blood neutrophils; this was not explained by changes in surface expression of Fas or by induction of Fas ligand. Inflammatory neutrophils remained sensitive to Fas‐induced death, at levels comparable to those seen in peripheral blood neutrophils. Similarly, granulocyte‐macrophage colony‐stimulating factor reduced apoptosis but did not abolish signaling via Fas. These data provide evidence for the rate of apoptosis in inflammatory neutrophils being continually modulated by death and survival signals in the inflammatory milieu. This allows for rapid resolution of inflammation as levels of survival factors fall, and suggests new strategies for inducing resolution of inflammation. J. Leukoc. Biol. 67: 662–668; 2000.