title: The glucocorticoid receptor in inflammatory processes: transrepression is not enough.
abstract: Glucocorticoids (GCs) are the most commonly used anti-inflammatory agents to treat inflammatory and immune diseases. However, steroid therapies are accompanied by severe side-effects during long-term treatment. The dogma that transrepression of genes, by tethering of the glucocorticoid receptor (GR) to DNA-bound pro-inflammatory transcription factors, is the main anti-inflammatory mechanism, is now challenged. Recent discoveries using conditional GR mutant mice and genomic approaches reveal that transactivation of anti-inflammatory acting genes is essential to suppress many inflammatory disease models. This novel view radically changes the concept to design selective acting GR ligands with a reduced side-effect profile.
authors.forename: Sabine
authors.initials: S
authors.lastname: Hübner
authors.forename: Lien
authors.initials: L
authors.lastname: Dejager
authors.forename: Claude
authors.initials: C
authors.lastname: Libert
authors.forename: Jan P
authors.initials: JP
authors.lastname: Tuckermann
mesh_terms: D000818:Animals; D015536:Down-Regulation / Q000235:genetics*; D006801:Humans; D007249:Inflammation / Q000235:genetics* / Q000276:immunology; D008024:Ligands; D011965:Receptors, Glucocorticoid / Q000235:genetics* / Q000378:metabolism; D015533:Transcriptional Activation / Q000235:genetics
chemical_list: D008024:Ligands; D011965:Receptors, Glucocorticoid