Type I interferon induction pathway, but not released interferon, participates in the maturation of dendritic cells induced by negative-strand RNA viruses

J Infect Dis. 2003 Apr 1;187(7):1126-36. doi: 10.1086/368381. Epub 2003 Mar 19.

Abstract

Signaling through toll-like receptors (TLRs) is essential for dendritic cell (DC) maturation induced by bacteria and other pathogens. The mechanism for virus-induced DC maturation is not known. By use of pairs of live viruses with different abilities to induce the interferon (IFN) pathway, a strong correlation between DC maturation and the ability of the virus to induce type I IFN synthesis was demonstrated. The secreted IFN was not necessary, nor was it sufficient to induce full DC maturation. Intracellular viral replication is necessary for this process, and the transcription factor nuclear factor-kappaB was crucial for cytokine induction. The double-stranded RNA-dependent protein kinase was not essential for DC maturation. Similar to TLR-induced DC maturation, after virus infection, separate pathways for the induction of cytokine secretion and the up-regulation of major histocompatibility complex and costimulatory molecules were activated. It was demonstrated that these pathways have different sensitivities to the presence of viral stimulus.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Cell Differentiation*
  • Cells, Cultured
  • Dendritic Cells / cytology*
  • Dendritic Cells / metabolism
  • Dendritic Cells / virology*
  • Dogs
  • Female
  • Gene Expression Regulation
  • Interferon Type I / immunology*
  • Interferon Type I / metabolism
  • Mice
  • NF-kappa B / metabolism
  • Orthomyxoviridae / immunology
  • RNA Viruses / immunology*
  • Sendai virus / immunology
  • Signal Transduction*
  • eIF-2 Kinase / metabolism

Substances

  • Interferon Type I
  • NF-kappa B
  • eIF-2 Kinase