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Reverse Signaling Through Transmembrane TNF Confers Resistance to Lipopolysaccharide in Human Monocytes and Macrophages

Günther Eissner, Silvia Kirchner, Heidrun Lindner, Walter Kolch, Petra Janosch, Matthias Grell, Peter Scheurich, Reinhard Andreesen and Ernst Holler
J Immunol June 15, 2000, 164 (12) 6193-6198; DOI: https://doi.org/10.4049/jimmunol.164.12.6193
Günther Eissner
*Department of Hematology and Oncology, University of Regensburg, Regensburg, Germany;
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Silvia Kirchner
*Department of Hematology and Oncology, University of Regensburg, Regensburg, Germany;
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Heidrun Lindner
*Department of Hematology and Oncology, University of Regensburg, Regensburg, Germany;
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Walter Kolch
†Beatson Institute for Cancer Research, Glasgow, United Kingdom; and
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Petra Janosch
†Beatson Institute for Cancer Research, Glasgow, United Kingdom; and
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Matthias Grell
‡Institute for Immunlogy and Cell Biology, University of Stuttgart, Stuttgart, Germany
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Peter Scheurich
‡Institute for Immunlogy and Cell Biology, University of Stuttgart, Stuttgart, Germany
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Reinhard Andreesen
*Department of Hematology and Oncology, University of Regensburg, Regensburg, Germany;
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Ernst Holler
*Department of Hematology and Oncology, University of Regensburg, Regensburg, Germany;
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Abstract

We have previously reported that the CD14+ monocytic subpopulation of human PBMC induces programmed cell death (apoptosis) in cocultured endothelial cells (EC) when stimulated by bacterial endotoxin (LPS). Apoptosis is mediated by two routes, first via transmembrane TNF-α (mTNF) expressed on PBMC and, in addition, by TNF-independent soluble factors that trigger apoptosis in EC. Neutralizing anti-TNF mAb completely blocked coculture-mediated apoptosis, despite the fact that there should have been additional soluble cell death factors. This led to the hypothesis that a reverse signal is transmitted from the TNF receptor on EC to monocytes (MO) via mTNF that prevents the production of soluble apoptotic factors. Here we have tested this hypothesis. The results support the idea of a bidirectional cross-talk between MO and EC. Peripheral blood MO, MO-derived macrophages (MΦ), or the monocytic cell line Mono Mac 6 were preincubated with human microvascular EC that constitutively express TNF receptor type I (TNF-R1) and subsequently stimulated with LPS. Cell-free supernatants of these preparations no longer induced EC apoptosis. The preincubation of MO/MΦ with TNF-reactive agents, such as mAb and soluble receptors, also blocked the production of death factors, providing further evidence for reverse signaling via mTNF. Finally, we show that reverse signaling through mTNF mediated LPS resistance in MO/MΦ as indicated by the down-regulation of LPS-induced soluble TNF and IL-6 as well as IL-1 and IL-10.

  • Received December 20, 1999.
  • Accepted April 3, 2000.
  • Copyright © 2000 by The American Association of Immunologists
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The Journal of Immunology: 164 (12)
The Journal of Immunology
Vol. 164, Issue 12
15 Jun 2000
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Reverse Signaling Through Transmembrane TNF Confers Resistance to Lipopolysaccharide in Human Monocytes and Macrophages
Günther Eissner, Silvia Kirchner, Heidrun Lindner, Walter Kolch, Petra Janosch, Matthias Grell, Peter Scheurich, Reinhard Andreesen, Ernst Holler
The Journal of Immunology June 15, 2000, 164 (12) 6193-6198; DOI: 10.4049/jimmunol.164.12.6193

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Reverse Signaling Through Transmembrane TNF Confers Resistance to Lipopolysaccharide in Human Monocytes and Macrophages
Günther Eissner, Silvia Kirchner, Heidrun Lindner, Walter Kolch, Petra Janosch, Matthias Grell, Peter Scheurich, Reinhard Andreesen, Ernst Holler
The Journal of Immunology June 15, 2000, 164 (12) 6193-6198; DOI: 10.4049/jimmunol.164.12.6193
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