作者: Masafumi Nakayama , Kazumi Ishidoh , Nobuhiko Kayagaki , Yuko Kojima , Noriko Yamaguchi
DOI: 10.4049/JIMMUNOL.168.2.734
关键词: Lysosome 、 Necrosis 、 Cell 、 Cytokine TWEAK 、 Programmed cell death 、 Cathepsin B 、 Cell culture 、 Biology 、 Apoptosis 、 Cell biology
摘要: TWEAK, a recently identified member of the TNF family, is expressed on IFN-γ-stimulated monocytes and induces cell death in certain tumor lines. In this study, we characterized TWEAK-induced several lines that exhibited distinct features. Although Kym-1 cells was indirectly mediated by TNF-α inhibited cycloheximide, HSC3 or IFN-γ-treated HT-29 not anti-TNF-α mAb suggesting direct triggering via TWEAK receptor latter The apoptosis associated with caspase-8 caspase-3 activation. pan-caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone, cells, it rather sensitized to necrosis. This necrosis abrogated lysosomal proteinase inhibitors, particularly cathepsin B [l-3- trans -(propylcarbamoyl)oxirane-2-carbonyl]-l-isoleucyl-l-proline methyl ester. During process necrosis, released from lysosome cytosol. DR3 has been reported be for all TWEAK-sensitive used study did express at either protein mRNA level, but bind CD8-TWEAK specifically. These results indicated could induce multiple pathways death, including both caspase-dependent B-dependent type-specific manner receptor(s) DR3.