Evidence map›Paper›PMID 27934944›Full record

ArticleScientific reports2016

Overexpression of Glucocorticoid-induced Leucine Zipper (GILZ) increases susceptibility to Imiquimod-induced psoriasis and involves cutaneous activation of TGF-β1.

Elena Carceller, Marlies Ballegeer, Julie Deckers, Carlo Riccardi, Stefano Bruscoli, Tino Hochepied, Claude Libert, Paloma Pérez

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 20 citations in OpenAlex.

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  8. Impaired estrogen signaling underlies regulatory T cell loss-of-function in the chronically inflamed intestine.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
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  10. Advances in Understanding the Immunological Pathways in Psoriasis.International journal of molecular sciences · 2019
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 3 countries.

Elena CarcellerInstituto de Biomedicina de Valencia-Consejo Superior de Investigaciones Científicas (IBV-CSIC), Jaime Roig 11, E-46010 Valencia, Spain.
Marlies BallegeerInflammation Research Center, VIB, B-9052 Ghent, Belgium.
Julie DeckersInflammation Research Center, VIB, B-9052 Ghent, Belgium.
Carlo RiccardiDepartment of Medicine, University of Perugia Medical School, 06132 Perugia, Italy.
Stefano BruscoliDepartment of Medicine, University of Perugia Medical School, 06132 Perugia, Italy.
Tino HochepiedInflammation Research Center, VIB, B-9052 Ghent, Belgium.
Claude LibertInflammation Research Center, VIB, B-9052 Ghent, Belgium.
Paloma PérezInstituto de Biomedicina de Valencia-Consejo Superior de Investigaciones Científicas (IBV-CSIC), Jaime Roig 11, E-46010 Valencia, Spain.
Ghent University · BEInstituto de Biomedicina de Valencia · ESUniversity of Perugia · ITVIB-UGent Center for Inflammation Research · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis vulgaris is a chronic inflammatory skin disease affecting millions of people. Its pathophysiology is complex and involves a skin compartment with epidermal and immune cells which produce cytokines, e.g. belonging to the IL-23-Th17-cell axis. Glucocorticoids (GCs) are the most common therapeutics used in cutaneous inflammatory disorders and GC-induced leucine zipper (GILZ) has emerged as a mediator of GCs due to its anti-inflammatory actions, theoretically lacking GC side-effects. We evaluated whether GILZ may provide a better therapeutic index in comparison to GCs during the onset and progression of psoriasis by generating and characterizing a mouse model with generalized overexpression of this protein (GILZ-Tg mice) and the imiquimod (IMQ) psoriasis model. Unexpectedly, in GILZ-Tg mice, the severity of IMQ-induced psoriasis-like skin lesions as well as induction of cytokines commonly up-regulated in human psoriasis (Il-17, Il-22, Il-23, Il-6, S100a8/a9, and Stat3) was significantly more pronounced relative to GILZ-Wt mice. The increased susceptibility to IMQ-induced psoriasis of GILZ-Tg mice was significantly associated with skin-specific over-activation of TGF-β1-mediated signaling via SMAD2/3. Our findings demonstrate that GILZ may behave as pro-inflammatory protein in certain tissues and that, similar to prolonged GC therapy, GILZ as an alternative treatment for psoriasis may also have adverse effects.

Indexed as

AminoquinolinesAnimalsCalgranulin ACytokinesDendritic CellsGene Expression RegulationGene Knock-In TechniquesImiquimodKeratinocytesMiceMice, Inbred C57BLMice, Inbred DBAMice, TransgenicNeutrophilsPsoriasisRecombinant ProteinsAminoquinolinesCalgranulin ACytokinesDsip1 protein, mouseImiquimodRecombinant ProteinsS100a8 protein, mouseSmad2 ProteinSmad2 protein, mouseSmad3 ProteinSmad3 protein, mouseTranscription FactorsTransforming Growth Factor beta1

Identifiers

PMID27934944
PMCPMC5146970
OpenAlexW2559939031

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.