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The Journal of Immunology, 2002, 169: 3120-3130.
Copyright © 2002 by The American Association of Immunologists

Regulation of IFN Regulatory Factor 4 Expression in Human T Cell Leukemia Virus-I-Transformed T Cells1

Sonia Sharma*,{dagger}, Nathalie Grandvaux*, Yael Mamane*,{dagger}, Pierre Genin*, Nazli Azimi{ddagger}, Thomas Waldmann{ddagger} and John Hiscott2,*,{dagger}

* Terry Fox Molecular Oncology Group, Lady Davis Institute for Medical Research, and {dagger} Department of Microbiology and Immunology, McGill University, Montreal, Canada; and {ddagger} National Cancer Institute, National Institutes of Health, Bethesda, MD 20892

IFN regulatory factor (IRF)-4 is a lymphoid/myeloid-restricted member of the IRF transcription factor family that plays an essential role in the homeostasis and function of mature lymphocytes. IRF-4 expression is tightly regulated in resting primary T cells and is transiently induced at the mRNA and protein levels after activation by Ag-mimetic stimuli such as TCR cross-linking or treatment with phorbol ester and calcium ionophore (PMA/ionomycin). However, IRF-4 is constitutively upregulated in human T cell leukemia virus type I (HTLV-I) infected T cells as a direct gene target for the HTLV-I Tax oncoprotein. In this study we demonstrate that chronic IRF-4 expression in HTLV-I-infected T lymphocytes is associated with a leukemic phenotype, and we examine the mechanisms by which continuous production of IRF-4 is achieved in HTLV-I-transformed T cells. IRF-4 expression in HTLV-1-infected cells is driven through activation of the NF-{kappa}B and NF-AT pathways, resulting in the binding of p50, p65, and c-Rel to the {kappa}B1 element and p50, c-Rel, and NF-ATp to the CD28RE element within the -617 to -209 region of the IRF-4 promoter. Furthermore, mutation of either the {kappa}B1 or CD28RE sites blocks Tax-mediated transactivation of the human IRF-4 promoter in T cells. These experiments constitute the first detailed analysis of human IRF-4 transcriptional regulation within the context of HTLV-I infection and transformation of CD4+ T lymphocytes.




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