Abstract:
:TWEAK is a recently cloned novel member of the TNF ligand family. Here we show that soluble TWEAK is sufficient to induce apoptosis in Kym-1 cells within 18 h. TWEAK-induced apoptosis is indirect and is mediated by the interaction of endogenous TNF and TNF receptor (TNFR)1, as each TNFR1-Fc, neutralizing TNF-specific antibodies and TNFR1-specific Fab fragments efficiently antagonize cell death induction. In addition to this indirect mode of action, co-stimulation of Kym-1 cells with TWEAK enhances TNFR1-mediated cell death induction. In contrast to TNF, TWEAK does only modestly activate NF-kappaB or c-jun N-terminal kinase (JNK) in Kym-1 cells. Although TWEAK binding to Kym-1 cells is easily detectable by flow cytometric analysis, we found neither evidence for expression of the recently identified TWEAK receptor Apo3/TRAMP/wsl/DR3/LARD, nor indications for direct interactions of TWEAK with TNFR. Together, these characteristics of TWEAK-induced signaling in Kym-1 cells argue for the existence of an additional, still undefined non-death domain-containing TWEAK receptor in Kym-1 cells.
journal_name
Eur J Immunoljournal_title
European journal of immunologyauthors
Schneider P,Schwenzer R,Haas E,Mühlenbeck F,Schubert G,Scheurich P,Tschopp J,Wajant Hdoi
10.1002/(SICI)1521-4141(199906)29:06<1785::AID-IMMkeywords:
subject
Has Abstractpub_date
1999-06-01 00:00:00pages
1785-92issue
6eissn
0014-2980issn
1521-4141journal_volume
29pub_type
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