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B RelA (p65) Is Essential for TNF-
-Induced Fas Expression but Dispensable for Both TCR-Induced Expression and Activation-Induced Cell Death1
*
Department of Biological Sciences, Columbia University, New York, NY 10027; and
Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia
The Fas death receptor plays a key role in the killing of target
cells by NK cells and CTLs and in activation-induced cell death of
mature T lymphocytes. These cytotoxic pathways are dependent on
induction of Fas expression by cytokines such as TNF-
and IFN-
or
by signals generated after TCR engagement. Although much of our
knowledge of the Fas death pathway has been generated from murine
studies, little is known about regulatory mechanisms important for
murine Fas expression. To this end, we have molecularly cloned a region
of the murine Fas promoter that is responsible for mediating TNF-
and PMA/PHA-induced expression. We demonstrate here that induction of
Fas expression by both stimuli is critically dependent on two sites
that associate with RelA-containing NF-
B complexes. To determine
whether RelA and/or other NF-B subunits are also important for
regulating Fas expression in primary T cells, we used CD4 T cells from
RelA-/-, c-Rel-/-, and p50-/-
mice. Although proliferative responses were significantly impaired,
expression of Fas and activation-induced cell death was unaffected in T
cells obtained from these different mice. Importantly, we show that
unlike fibroblasts, which consist primarily of RelA-containing NF-B
complexes, T cells have high levels of both RelA and c-Rel complexes,
suggesting that Fas expression in T cells may be dependent on redundant
functions of these NF-B subunits.
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