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B Signaling Reveals a Novel Role for NF-B in the Regulation of TNF-Related Apoptosis-Inducing Ligand Expression1
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,,,
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Terry Fox Molecular Oncology Group,
Lady Davis Institute for Medical Research, and Departments of
Microbiology and Immunology and
Medicine and Oncology, McGill University, Montreal, Canada
The NF-
B family of transcription factors functions broadly in
the host control of immunoregulatory gene expression, inflammation, and
apoptosis. Using Jurkat T cells engineered to inducibly express a
transdominant repressor of IB
, we examined the role of NF-B in
the regulation of cytokine and apoptotic gene expression. In this T
cell model, as well as in primary T lymphocytes, expression of
TNF-related apoptosis-inducing ligand (TRAIL) apoptotic signaling
protein was dramatically down-regulated by inhibition of NF-B
binding activity. TRAIL acts through membrane death receptors to induce
apoptosis of activated T lymphocytes and can be up-regulated by a
variety of physiological and pharmacological inducers. However,
regulation of TRAIL gene expression has not been defined. Treatment
with TCR mimetics (PMA/ionomycin, PHA, and anti-CD3/CD28 Abs)
resulted in a rapid increase in the expression of TRAIL mRNA and cell
surface TRAIL protein. Induction of the transdominant repressor of
IB dramatically down-regulated surface expression of TRAIL,
indicating an essential role for NF-B in the regulation of TRAIL.
The induced expression of TRAIL was linked to a c-Rel binding
site in the proximal TRAIL promoter at position -256 to -265;
mutation of this site or an adjacent B site resulted in a complete
loss of the inducibility of the TRAIL promoter. The regulation of TRAIL
expression by NF-B may represent a general mechanism that
contributes to the control of TRAIL-mediated apoptosis in T
lymphocytes.
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