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J Biol Chem, Vol. 274, Issue 41, 28916-28921, October 8, 1999
,,,
From the Tumor necrosis factor-related apoptosis-inducing
ligand (TRAIL), a new member of the tumor necrosis factor (TNF) family,
induces apoptosis primarily of transformed cells. Interleukin-1 was
previously found to protect the keratinocyte cell line KB from
TRAIL-induced apoptosis, thus we studied whether interleukin-1 also
protects from other apoptotic stimuli (ultraviolet radiation (UV),
CD95-ligand). Interleukin-1 rescued KB cells from TRAIL- and
CD95-induced apoptosis, which was critically dependent on nuclear
factor Ludwig Boltzmann Institute for Cell Biology
and Immunobiology of the Skin, Department of Dermatology, University of
Münster, Von-Esmarchstrasse 56, D-48149 Münster, Germany
and § Immunex Corporation, Seattle, Washington 98101
B, because cells transfected with a super-repressor form of
the nuclear factor B inhibitor IB were less protected. In
contrast, UV-mediated apoptosis was not only not prevented by
interleukin-1 but even enhanced. This opposite effect of interleukin-1
was also observed for the expression of the inhibitor of apoptosis
proteins (IAP). Whereas TRAIL- and CD95-mediated suppression of IAP
expression was partially reversed by interleukin-1, UV-mediated
down-regulation of IAPs was not reversed but even further enhanced.
Increased apoptosis induced by interleukin-1 plus UV was accompanied by excessive TNF
release, implying that enhanced cytotoxicity is due to
the additive effect of these two apoptotic stimuli. Accordingly, enhanced apoptosis was reduced by blocking the TNF receptor-1. The
opposite effects of interleukin-1 indicate that different mechanisms
are involved in UV-induced apoptosis compared with CD95- and
TRAIL-mediated apoptosis. Furthermore, the data suggest that whether a
signal acts in an antiapoptotic way or not does not only depend on the
signal itself but also on the stimulus causing apoptosis.
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