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Viral IFN-Regulatory factors inhibit activation-induced cell death via two positive regulatory IFN-regulatory factor 1-dependent domains in the CD95 ligand Promoter

The CD95 (also called APO-1/Fas) system plays a major role in the induction of apoptosis in lymphoid and nonlymphoid tissues. The CD95 ligand (CD95L) is induced in response to a variety of signals, including IFN-γ and TCR/CD3 stimulation. Here we report the identification of two positive regulatory...

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Hauptverfasser: Kirchhoff, Sabine (VerfasserIn) , Li-Weber, Min (VerfasserIn) , Krammer, Peter H. (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: February 1, 2002
In: The journal of immunology
Year: 2002, Jahrgang: 168, Heft: 3, Pages: 1226-1234
ISSN:1550-6606
DOI:10.4049/jimmunol.168.3.1226
Online-Zugang:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.4049/jimmunol.168.3.1226
Verlag, lizenzpflichtig, Volltext: https://www.jimmunol.org/content/168/3/1226
Volltext
Verfasserangaben:Sabine Kirchhoff, Thorsten Sebens, Sven Baumann, Andreas Krueger, Rainer Zawatzky, Min Li-Weber, Edgar Meinl, Frank Neipel, Bernhard Fleckenstein, and Peter H. Krammer
Beschreibung
Zusammenfassung:The CD95 (also called APO-1/Fas) system plays a major role in the induction of apoptosis in lymphoid and nonlymphoid tissues. The CD95 ligand (CD95L) is induced in response to a variety of signals, including IFN-γ and TCR/CD3 stimulation. Here we report the identification of two positive regulatory IFN-regulatory factor-dependent domains (PRIDDs) in the CD95L promoter and its 5′ untranslated region, respectively. EMSAs demonstrate specific binding of IFN-γ-induced IFN-regulatory factor 1 (IRF-1) to the PRIDD sequences. Ectopic IRF-1 expression induces CD95L promoter activity. Furthermore, we demonstrate that PRIDDs play an important role in TCR/CD3-mediated CD95L induction. Most interestingly, viral IRFs of human herpes virus 8 (HHV8) totally abolish IRF-1-mediated and strongly reduce TCR/CD3-mediated CD95L induction. We demonstrate here for the first time that viral IRFs inhibit activation-induced cell death. Thus, these results demonstrate an important mechanism of HHV8 to modulate the immune response by down-regulation of CD95L expression. Inhibition of CD95-dependent T cell function might contribute to the immune escape of HHV8.
Beschreibung:Gesehen am 15.04.2021
Beschreibung:Online Resource
ISSN:1550-6606
DOI:10.4049/jimmunol.168.3.1226

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