IRF-3-dependent and augmented target genes during viral infection

Genes Immun. 2008 Mar;9(2):168-75. doi: 10.1038/sj.gene.6364449. Epub 2007 Dec 20.

Abstract

Activation of the transcription factor interferon regulatory factor-3 (IRF-3) is an essential event in the innate immune response to viral infection. To understand the contribution of IRF-3 to host defense, we used a systems biology approach to analyze global gene expression dependent on IRF-3. Comparison of expression profiles in cells from IRF-3 knockout animals or wild-type siblings following viral infection revealed three sets of induced genes, those that are strictly dependent on IRF-3, augmented with IRF-3, or not responsive to IRF-3. Products of identified IRF-3 target genes are involved in innate or acquired immunity, or in the regulation of cell cycle, apoptosis and proliferation. These results reveal the global effects of one transcription factor in the immune response and provide information to evaluate the integrated response to viral infection.

Publication types

  • Comparative Study
  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Cells, Cultured
  • Gene Expression Profiling* / methods
  • Gene Expression Regulation, Viral / genetics
  • Gene Targeting / methods*
  • Immunity, Innate / genetics
  • Interferon Regulatory Factor-3 / deficiency
  • Interferon Regulatory Factor-3 / genetics*
  • Interferon Regulatory Factor-3 / physiology
  • Mice
  • Mice, Knockout
  • Newcastle Disease / genetics*
  • Newcastle Disease / virology
  • Newcastle disease virus / genetics
  • Oligonucleotide Array Sequence Analysis
  • Transcription Factors / biosynthesis
  • Transcription Factors / genetics
  • Transcription Factors / metabolism

Substances

  • ISG54 protein, mouse
  • Interferon Regulatory Factor-3
  • Irf3 protein, mouse
  • Transcription Factors