Differential expression of Fas (CD95) and Fas ligand on normal human phagocytes: implications for the regulation of apoptosis in neutrophils

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Differential expression of Fas (CD95) and Fas ligand on normal human phagocytes: implications for the regulation of apoptosis in neutrophils

WC Liles, PA Kiener, JA Ledbetter, A Aruffo and SJ Klebanoff
Department of Medicine, University of Washington, Seattle 98195-7185, USA.

Human neutrophils, monocytes, and eosinophils are known to undergo apoptotic cell death. The Fas/Fas ligand pathway has been implicated as an important cellular pathway mediating apoptosis in diverse cell types. We conducted studies to examine the importance of the Fas/FasL system in normal human phagocytes. Although Fas expression was detected on neutrophils, monocytes, and eosinophils, constitutive expression of FasL was restricted to neutrophils. The three types of phagocytes demonstrated differential sensitivity to Fas-induced apoptosis. Only neutrophils were highly susceptible to rapid apoptosis in vitro after stimulation with activating anti-Fas IgM (mAb CH-11). Fas-mediated neutrophil apoptosis was suppressed by incubation with G-CSF, GM-CSF, IFN-gamma, TNF-alpha, or dexamethasone, as well as the selective tyrosine kinase inhibitors, herbimycin A and genistein. Spontaneous neutrophil death in vitro was partially suppressed by Fas-Ig fusion protein or antagonistic anti-Fas IgG1 (mAb ZB4). In coculture experiments, neutrophils released a soluble factor inducing death in Fas-susceptible Jurkat cells via a mechanism sensitive to the presence of Fas-Ig or anti-Fas IgG1. Immunoblot analysis using specific anti- human FasL IgG1 (mAb No. 33) identified a 37-kD protein in lysates of freshly isolated neutrophils and a 30-kD protein in the culture supernatant of neutrophils maintained in vitro. Our results suggest that mature neutrophils may be irrevocably committed to autocrine death by virtue of their constitutive coexpression of cell-surface Fas and FasL via a mechanism that is sensitive to proinflammatory cytokines, glucocorticoids, and inhibitors of tyrosine kinase activity. Furthermore, neutrophils can serve as a source of soluble FasL, which may function in a paracrine pathway to mediate cell death.
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Schwarzenberger, P., Huang, W., Ye, P., Oliver, P., Manuel, M., Zhang, Z., Bagby, G., Nelson, S., Kolls, J. K. (2000). Requirement of Endogenous Stem Cell Factor and Granulocyte-Colony-Stimulating Factor for IL-17-Mediated Granulopoiesis. J. Immunol. 164: 4783-4789 [Abstract] [Full Text]
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Schneider, D. B., Vassalli, G., Wen, S., Driscoll, R. M., Sassani, A. B., DeYoung, M. B., Linnemann, R., Virmani, R., Dichek, D. A. (2000). Expression of Fas Ligand in Arteries of Hypercholesterolemic Rabbits Accelerates Atherosclerotic Lesion Formation. Arterioscler. Thromb. Vasc. Bio. 20: 298-308 [Abstract] [Full Text]
HASHIMOTO, S., KOBAYASHI, A., KOOGUCHI, K., KITAMURA, Y., ONODERA, H., NAKAJIMA, H. (2000). Upregulation of Two Death Pathways of Perforin/Granzyme and FasL/Fas in Septic Acute Respiratory Distress Syndrome. Am. J. Respir. Crit. Care Med. 161: 237-243 [Abstract] [Full Text]
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Aprikyan, A. A. G., Liles, W. C., Park, J. R., Jonas, M., Chi, E. Y., Dale, D. C. (2000). Myelokathexis, a congenital disorder of severe neutropenia characterized by accelerated apoptosis and defective expression of bcl-x in neutrophil precursors. Blood 95: 320-327 [Abstract] [Full Text]
Tanner, J. E., Alfieri, C. (1999). Epstein-Barr Virus Induces Fas (CD95) in T Cells and Fas Ligand in B Cells Leading to T-Cell Apoptosis. Blood 94: 3439-3447 [Abstract] [Full Text]
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Chen, X.-M., Gores, G. J., Paya, C. V., LaRusso, N. F. (1999). Cryptosporidium parvum induces apoptosis in biliary epithelia by a Fas/Fas ligand-dependent mechanism. Am. J. Physiol. Gastrointest. Liver Physiol. 277: G599-G608 [Abstract] [Full Text]
Matute-Bello, G., Liles, W. C., Steinberg, K. P., Kiener, P. A., Mongovin, S., Chi, E. Y., Jonas, M., Martin, T. R. (1999). Soluble Fas Ligand Induces Epithelial Cell Apoptosis in Humans with Acute Lung Injury (ARDS). J. Immunol. 163: 2217-2225 [Abstract] [Full Text]
O'Connell, J., Bennett, M. W., O'Sullivan, G. C., O'Callaghan, J., Collins, J. K., Shanahan, F. (1999). Expression of Fas (CD95/APO-1) Ligand by Human Breast Cancers: Significance for Tumor Immune Privilege. CVI 6: 457-463 [Abstract] [Full Text]
Khwaja, A., Tatton, L. (1999). Caspase-Mediated Proteolysis and Activation of Protein Kinase Cdelta Plays a Central Role in Neutrophil Apoptosis. Blood 94: 291-301 [Abstract] [Full Text]