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Papers In Press, published online ahead of print August 11, 2004
Oncology Center, The Johns Hopkins University, Baltimore, MD 21231-1001
Corresponding Author: parowe{at}jhmi.edu
The interferon regulatory factors (IRF) are transcriptional mediators of cellular response to viral invasion that play a critical role in the innate antiviral defense. Two of these factors, IRF-5 and IRF-7, play a critical role in the induction of interferon (IFNA) genes in infected cells; they are expressed constitutively in monocytes, B cells and high producers of interferon alpha-precursors of dendritic cells (pDC2), and their expression can be further stimulated by Type I IFN. The goal of the present study was to identify and analyze expression of cellular genes that are modulated by IRF-5 and IRF-7 during the innate response to viral infection. The transcription profiles of infected BJAB cells overexpressing IRF-5 or IRF-7 were determined by using oligonucleotide arrays with probe sets representing about 6800 human genes. This analysis shows that IRF-5 and IRF-7 activate a broad profile of heterologous genes encoding not only antiviral, inflammatory and pro-apoptotic proteins, but also proteins of other functional categories. The number of IRF-5 and IRF-7 modulated genes was significantly higher in infected than in uninfected cells and the transcription signature was predominantly positive. Although IRF-5 and IRF-7 stimulated a large number of common genes, a distinct functional profile was associated with each of these IRFs. The noted difference was a broad antiviral and early inflammatory transcriptional profile in infected BJAB/IRF-5 cells while the IRF-7 induced transcripts were enriched for the group of mitochondrial genes and genes affecting the DNA structure. Taken together, these data indicate that IRF-5 and IRF-7 act primarily as transcriptional activators and that IRF-5 and IRF-7- induced innate antiviral response results in a broad alteration of the transcriptional profile of cellular genes.
J. Biol. Chem, 10.1074/jbc.M400726200
Submitted on January 22, 2004
Revised on August 11, 2004
Accepted on August 11, 2004
Global and specific targets of IRF-5 and IRF-7 during innate response to viral infection
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