The role of STAT1 in viral sensitization to LPS

Joan Durbin, Leslie Doughty, Ken Nguyen, Michael Caligiuri, Jeff Van Deusen, Christine Biron

Research output: Contribution to journalArticlepeer-review

8 Scopus citations


The phenomenon of endotoxin sensitization by virus infection is well documented but not yet well understood. Infection by virtually any viral agent will quickly induce expression of type I interferons (IFN-α/β), and type II IFN-γ production will follow as NK cells and T cells are activated. It has been well established that type II IFN pretreatment can intensify the effects of endotoxin. We have recently demonstrated that type I IFN induction by lymphocytic choriomeningitis virus (LCMV) infection dramatically increases TNF-α production following LPS treatment, and that this sensitization by type I IFN is STAT1 dependent. Taken together these data suggest that the STAT1-mediated, MyD88-independent, arm of the LPS signaling pathway plays an important role in endotoxin toxicity, and that this pathway mediates a major component of virus-enhanced LPS sensitization.

Original languageEnglish (US)
Pages (from-to)313-316
Number of pages4
JournalJournal of Endotoxin Research
Issue number5
StatePublished - 2003
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Immunology
  • Toxicology


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