Glucocorticoid-induced leucine zipper (GILZ) in immuno suppression: master regulator or bystander?
Induction of glucocorticoid-induced leucine zipper (GILZ) by glucocorticoids has been reported to be essential for their anti-inflammatory actions. At the same time, GILZ is actively downregulated under inflammatory conditions, resulting in an enhanced pro-inflammatory response. Two papers published in the recent past showed elevated GILZ expression in the late stage of an inflammation. Still, the manuscripts suggest seemingly contradictory roles of endogenous GILZ: one of them suggested compensatory actions by elevated corticosterone levels in GILZ knockout mice, while our own manuscript showed a distinct phenotype upon GILZ knockout in vivo. Herein, we discuss the role of GILZ in inflammation with a special focus on the influence of endogenous GILZ on macrophage responses and suggest a cell-type specific action of GILZ as an explanation for the conflicting results as presented in recent reports.
Department of Pharmacy, Pharmaceutical Biology, Saarland University, Saarbrücken, Germany.
Jessica
J
Hoppstädter
Department of Pharmacy, Pharmaceutical Biology, Saarland University, Saarbrücken, Germany.
Alexandra K
AK
Kiemer
D000818:Animals; D004195:Disease Models, Animal; D005938:Glucocorticoids / Q000276:immunology / Q000494:pharmacology; D006801:Humans; D007249:Inflammation / Q000276:immunology; D016350:Leucine Zippers / Q000276:immunology*; D008070:Lipopolysaccharides / Q000276:immunology / Q000494:pharmacology; D008264:Macrophages / Q000276:immunology; D051379:Mice; D018345:Mice, Knockout; D014157:Transcription Factors / Q000276:immunology*
C498608:Dsip1 protein, mouse; D005938:Glucocorticoids; D008070:Lipopolysaccharides; C404226:TSC22D3 protein, human; D014157:Transcription Factors
glucocorticoids; inflammation; lipopolysaccharide; macrophage; mouse models