Research Perspectives:

Glucocorticoid-induced leucine zipper (GILZ) in immuno suppression: master regulator or bystander?

Jessica Hoppstädter _ and Alexandra K. Kiemer

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Oncotarget. 2015; 6:38446-38457. https://doi.org/10.18632/oncotarget.6197

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Jessica Hoppstädter1 and Alexandra K. Kiemer1

1 Department of Pharmacy, Pharmaceutical Biology, Saarland University, Saarbrücken, Germany

Correspondence to:

Jessica Hoppstädter, email:

Keywords: inflammation, macrophage, lipopolysaccharide, glucocorticoids, mouse models

Received: August 31, 2015 Accepted: October 12, 2015 Published: October 20, 2015


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.

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