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...

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Bibliographic Details
Published in:Oncotarget 2015-11, Vol.6 (36), p.38446-38457
Main Authors: Hoppstädter, Jessica, Kiemer, Alexandra K
Format: Article
Language:English
Subjects:
Animals
Disease Models, Animal
Glucocorticoids - immunology
Glucocorticoids - pharmacology
Humans
Inflammation - immunology
Leucine Zippers - immunology
Lipopolysaccharides - immunology
Lipopolysaccharides - pharmacology
Macrophages - immunology
Mice
Mice, Knockout
Transcription Factors - immunology
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Summary: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.
ISSN:1949-2553
1949-2553
DOI:10.18632/oncotarget.6197