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Promoter1
* Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892; and
Terry Fox Molecular Oncology Group, Lady Davis Institute for Medical Research, and Departments of Microbiology and Immunology, Medicine, and Oncology, McGill University, Montreal, Canada
IL-15R
mRNA and protein levels are increased in human T cell
lymphotropic virus type-I (HTLV-I)-associated adult T cell leukemia.
Previously, we demonstrated that IL-15R expression was activated by
HTLV-I Tax, in part, through the action of NF-
B. However, there
appeared to be additional motifs within the IL-15R promoter that
were responsive to HTLV-I Tax. In this study, we demonstrated that
IL-15R mRNA expression was activated in human monocytes by IFN
treatment, suggesting a role for IFN regulatory factors (IRFs) in
IL-15R transcription. In addition, an IRF element within the
Tax-responsive element of the IL-15R promoter was necessary for
maximal Tax-induced activation of this promoter. Furthermore, we
demonstrated that IRF-4, a transcription factor known to be elevated in
HTLV-I-infected cells, activated the IL-15R promoter. Inhibition of
IRF-4 action lead to reduced Tax-induced activation of the IL-15R
promoter, while inhibition of both IRF-4 and NF-B severely inhibited
the Tax-induced activation of this promoter. These findings suggest a
role for both NF-B and IRF-4 in the transcriptional regulation of
IL-15R by HTLV-I Tax. It is possible that the HTLV-I Tax-mediated
induction of IL-15R and IL-15 may lead to an autocrine
cytokine-mediated stimulatory loop leading to the proliferation of
HTLV-I infected cells. This loop of proliferation may facilitate viral
propagation and play a role in HTLV-I-mediated disease
progression.
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