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Gene Expression Through an NF-
B Site
*
Metabolism Branch, Division of Clinical Sciences, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892; and
Graduate Genetics Program, Institute of Biomedical Sciences, George Washington University, Washington, DC 20052
IL-15 mRNA levels are increased in diseases caused by human T cell
lymphotropic virus type I (HTLV-I). In this study, we demonstrated that
IL-15R
, the IL-15-specific binding receptor, mRNA and protein levels
were also elevated in HTLV-I-infected cells. We showed that transient
HTLV-I Tax expression lead to increased IL-15R mRNA levels. In
addition, by using a reporter construct that bears the human IL-15R
promoter, we demonstrated that Tax expression increased promoter
activity by at least 4-fold. Furthermore, using promoter deletion
constructs and gel shift analysis, we defined a functional
NF-
B-binding motif in the human IL-15R promoter, suggesting that
Tax activation of IL-15R is due, in part, to the induction of
NF-B. These data indicate that IL-15R is transcriptionally
regulated by the HTLV-I Tax protein through the action of NF-B.
These findings suggest a role for IL-15R in aberrant T cell
proliferation observed in HTLV-I-associated
diseases.
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