Inflammation suppressor genes: Please switch out all the lights

Christine A. Wells, Timothy Ravasi, David A. Hume*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

75 Scopus citations

Abstract

An effective immune system requires rapid and appropriate activation of inflammatory mechanisms but equally rapid and effective resolution of the inflammatory state. A review of the canonical host response to gram-negative bacteria, the lipopolysaccharide-Toll-like receptor 4 signaling cascade, highlights the induction of repressors that act at each step of the activation process. These inflammation suppressor genes are characterized by their induction in response to pathogen, typically late hi the macrophage activation program, and include an expanding class of dominant-negative proteins derived from alternate splicing of common signaling components. Despite the expanse of anti-inflammatory mechanisms available to an activated macrophage, the frailty of this system is apparent in the large numbers of genes implicated in chronic inflammatory diseases. This apparent lack of redundancy between inflammation suppressor genes is discussed with regard to evolutionary benefits in generating a heterogeneous population of immune cells and consequential robustness hi defense against new and evolving pathogens.

Original languageEnglish (US)
Pages (from-to)9-13
Number of pages5
JournalJournal of Leukocyte Biology
Volume78
Issue number1
DOIs
StatePublished - Jul 1 2005

Keywords

  • Lipopolysaccharide
  • Macrophage
  • Toll-like receptor

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Cell Biology

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