Modulation of acute and chronic inflammation of the lung by GITR and its ligand

Ann N Y Acad Sci. 2007 Jun:1107:380-91. doi: 10.1196/annals.1381.040.

Abstract

Glucocorticoid-induced TNFR-related (GITR) protein, a member of the tumor necrosis factor receptor superfamily, is expressed in many components of the innate and adaptive immune system and modulates their activation following interaction with its ligand (GITRL). Here we review and discuss results described in previous publications where the role of the GITR/GITRL system in lung inflammation was evaluated using two experimental systems. We also discuss the proinflammatory role played by the GITR/GITRL system and the potential use of GITR fusion protein in inhibiting inflammation.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Acute Disease
  • Animals
  • Chronic Disease
  • Glucocorticoid-Induced TNFR-Related Protein / metabolism*
  • Humans
  • Ligands
  • Pneumonia / immunology
  • Pneumonia / metabolism*
  • Pneumonia / pathology*
  • Tumor Necrosis Factors / metabolism*

Substances

  • Glucocorticoid-Induced TNFR-Related Protein
  • Ligands
  • Tumor Necrosis Factors