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Blood, Vol. 95 No. 11 (June 1), 2000:
pp. 3478-3482
Expression of c-FLIPL and resistance to CD95-mediated
apoptosis of monocyte-derived dendritic cells: inhibition by
bisindolylmaleimide
Fabienne Willems,
Zoulikha Amraoui,
Nathalie Vanderheyde,
Valérie Verhasselt,
Ezra Aksoy,
Carsten Scaffidi,
Marcus E. Peter,
Peter H. Krammer, and
Michel Goldman
From the Laboratory of Experimental Immunology, Université
Libre de Bruxelles, Brussels, Belgium, and the German Cancer Research
Center, Tumor Immunology Program, Heidelberg, Germany.
To gain insight into the mechanisms controlling apoptosis of
dendritic cells (DC), human monocyte-derived DC were analyzed for their
expression of CD95 (Fas/Apo-1) and their response to CD95 ligation.
Although DC expressed the CD95 molecule on their membrane, they did not
undergo apoptosis on CD95 ligation unless sensitized by cycloheximide.
In parallel, DC synthesized c-FLIPL, an inhibitor of the
CD95-mediated death-signaling cascade. We also demonstrated that
bisindolylmaleimide down-regulates c-FLIPL expression in DC
and, in parallel, allows CD95-mediated apoptosis in these cells. In
contrast, Bcl-2, Bcl-xL, and Bax levels were
not affected by bisindolylmaleimide. We conclude that DC resist
CD95- mediated apoptosis in association with c-FLIPL
expression and that the immunosuppressive potential of
bisindolylmaleimide previously observed at the T-cell level also
involves facilitation of CD95-mediated DC apoptosis.
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