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*
Tumor Immunology Program,
Tumorvirus-Immunology, German Cancer Research Center, Heidelberg, Germany;
Department of Neuroimmunology, Max Planck Institute of Neurobiology, Martinsried, Germany;
Institute for Clinical Neuroimmunology, Ludwig Maximilians University, Munich, Germany; and
¶
Institute for Clinical and Molecular Virology, University Erlangen-Nürnberg, Erlangen-Nürnberg, Germany
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-
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--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.
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