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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Human T cell lymphotropic virus type I Tax activates IL-15R alpha gene expression through an NF-kappa B site.

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-15Ralpha, 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-15Ralpha mRNA levels. In addition, by using a reporter construct that bears the human IL-15Ralpha 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-kappaB-binding motif in the human IL-15Ralpha promoter, suggesting that Tax activation of IL-15Ralpha is due, in part, to the induction of NF-kappaB. These data indicate that IL-15Ralpha is transcriptionally regulated by the HTLV-I Tax protein through the action of NF-kappaB. These findings suggest a role for IL-15Ralpha in aberrant T cell proliferation observed in HTLV-I-associated diseases.[1]

References

  1. Human T cell lymphotropic virus type I Tax activates IL-15R alpha gene expression through an NF-kappa B site. Mariner, J.M., Lantz, V., Waldmann, T.A., Azimi, N. J. Immunol. (2001) [Pubmed]
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