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• W2132439466 abstract "Abstract. Objective : Two types of interferons (IFNs), type I (IFN‐α/β) and type III (IFN‐λs), utilize distinct receptor complexes to induce similar signalling and biological activities, including recently demonstrated for IFN‐λs antitumour activity. However, ability of type III IFNs to regulate cell population growth remains largely uncharacterized. Materials and methods : Intact and modified human colorectal adenocarcinoma HT29 cells were used to study regulation of apoptosis by IFN‐λs. Results and Conclusions : We report that the IFN‐λR1 chain of the type III IFN receptor complex possesses an intrinsic ability to trigger apoptosis in cells. Signalling induced through the intracellular domain of IFN‐λR1 resulted in G 1 /G 0 phase cell cycle arrest, phosphatidylserine surfacing and chromosomal DNA fragmentation. Caspase‐3, caspase‐8 and caspase‐9 were activated; however, pancaspase inhibitor Z‐VAD‐FMK did not prevent apoptosis. In addition, the extent of apoptosis correlated with the level of receptor expression and was associated with prolonged IFN‐λ signalling. We also demonstrated that the ability to trigger apoptosis is a unique intrinsic function of all IFN receptors. However, more robust apoptosis was induced by signalling through type III IFN receptor than through type I or type II (IFN‐γ) receptors, suggesting higher cytotoxic potential of type III IFNs. In addition, we observed that IFN‐γ treatment sensitized HT29 cells to IFN‐λ‐mediated apoptosis. These results provide evidence that type III IFNs, alone or in combination with other stimuli, have the potential to induce apoptosis." @default.
• W2132439466 created "2016-06-24" @default.
• W2132439466 creator A5020001279 @default.
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• W2132439466 creator A5066532132 @default.
• W2132439466 creator A5085610468 @default.
• W2132439466 date "2008-11-18" @default.
• W2132439466 modified "2023-10-17" @default.
• W2132439466 title "Regulation of apoptosis by type III interferons" @default.
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• W2132439466 doi "https://doi.org/10.1111/j.1365-2184.2008.00558.x" @default.
• W2132439466 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6496378" @default.
• W2132439466 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19040572" @default.
• W2132439466 hasPublicationYear "2008" @default.
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