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• W2143200082 abstract "Several combined strategies have been recently proposed to overcome the resistance to tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) showed by some tumor cells, thus improving the use of this death ligand in antitumor therapy. However, the molecular mechanisms of the tumor selective activity of TRAIL are not completely understood and hence the effects of the combined therapy on normal cells are unknown. Here, we have studied the resistance of primary T lymphocytes to TRAIL-mediated apoptosis. No significant differences were found in the expression of proteins involved in TRAIL-mediated apoptosis between resting and activated T cells. The low expression of death receptors TRAIL-R1/-R2 as well as the high levels of the antiapoptotic proteins TRAIL-R4 and cellular Fas-associated death domain-like IL-1β-converting enzyme-inhibitory protein (c-FLIP) may explain the lack of caspase-8 activation observed upon TRAIL treatment in both cell types. We have also analyzed the effect of different sensitizing agents such as genotoxic drugs, phosphatidylinositol-3 kinase (PI3K) inhibitors, proteasome inhibitors, microtubule depolymerizing agents, histone deacetilase inhibitors (HDACi), and NF-κB inhibitors. Although some of them induced T cell death, only NF-κB inhibitors sensitized activated T cells to TRAIL-induced apoptosis, maybe through the regulation of the antiapoptotic proteins TRAIL-R4, c-FLIPS and members of the inhibitors of apoptosis proteins (IAP) family. These results question the safety of the combined treatments with TRAIL and NF-κB inhibitors against tumors." @default.
• W2143200082 created "2016-06-24" @default.
• W2143200082 creator A5039618938 @default.
• W2143200082 creator A5059527055 @default.
• W2143200082 creator A5060889102 @default.
• W2143200082 date "2007-04-01" @default.
• W2143200082 modified "2023-10-17" @default.
• W2143200082 title "Regulation of the resistance to TRAIL-induced apoptosis in human primary T lymphocytes: Role of NF-κB inhibition" @default.
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• W2143200082 doi "https://doi.org/10.1016/j.molimm.2006.12.015" @default.
• W2143200082 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17257681" @default.
• W2143200082 hasPublicationYear "2007" @default.
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