Eissner, Guenther and Kirchner, Silvia and Lindner, Heidrun and Kolch, Walter and Janosch, Petra and Grell, Matthias and Scheurich, Peter and Andreesen, Reinhard and Holler, Ernst (2000) Reverse signaling through transmembrane TNF confers resistance to lipopolysaccharide in human monocytes and macrophages. JOURNAL OF IMMUNOLOGY, 164 (12). pp. 6193-6198. ISSN 0022-1767
Full text not available from this repository. (Request a copy)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-alpha (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 (M Phi), 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/M Phi 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/M Phi as indicated by the down-regulation of LPS-induced soluble TNF and IL-6 as well as IL-1 and IL-10.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | TUMOR-NECROSIS-FACTOR; FACTOR-ALPHA; LIGAND; APOPTOSIS; RESPONSES; RECEPTOR; CELLS; MATURATION; CYTOLYSIS; FAMILY; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Innere Medizin III (Hämatologie und Internistische Onkologie) |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 05 Apr 2022 13:16 |
| Last Modified: | 05 Apr 2022 13:16 |
| URI: | https://pred.uni-regensburg.de/id/eprint/42405 |
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