Evidence map›Paper›PMID 24587313›Full record

ArticlePloS one2014

IL-17 induces an expanded range of downstream genes in reconstituted human epidermis model.

Andrea Chiricozzi, Kristine E Nograles, Leanne M Johnson-Huang, Judilyn Fuentes-Duculan, Irma Cardinale, Kathleen M Bonifacio, Nicholas Gulati, Hiroshi Mitsui, Emma Guttman-Yassky, Mayte Suárez-Fariñas and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 2 pooled it
8.1field-weighted citation impact, top 2% 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

86 citing papers in PubMed, 2 syntheses or guidelines pooled it, 177 citations in OpenAlex.

  1. Pooled it
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  10. The Immunology of Psoriasis-Current Concepts in Pathogenesis.Clinical reviews in allergy & immunology · 2024
    Review
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26 more citing papers are in PubMed but not listed here.

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

11 authors at 2 institutions in 2 countries.

Andrea ChiricozziLaboratory for Investigative Dermatology, The Rockefeller University, New York City, New York, United States of America ; Center for Clinical and Translational Science, The Rockefeller University, New York City, New York, United States of America ; Department of Dermatology, University of Rome "Tor Vergata", Rome, Italy.
Kristine E NogralesLaboratory for Investigative Dermatology, The Rockefeller University, New York City, New York, United States of America ; Center for Clinical and Translational Science, The Rockefeller University, New York City, New York, United States of America.
Leanne M Johnson-HuangLaboratory for Investigative Dermatology, The Rockefeller University, New York City, New York, United States of America.
Judilyn Fuentes-DuculanLaboratory for Investigative Dermatology, The Rockefeller University, New York City, New York, United States of America.
Irma CardinaleLaboratory for Investigative Dermatology, The Rockefeller University, New York City, New York, United States of America.
Kathleen M BonifacioLaboratory for Investigative Dermatology, The Rockefeller University, New York City, New York, United States of America.
Nicholas GulatiLaboratory for Investigative Dermatology, The Rockefeller University, New York City, New York, United States of America.
Hiroshi MitsuiLaboratory for Investigative Dermatology, The Rockefeller University, New York City, New York, United States of America.
Emma Guttman-YasskyLaboratory for Investigative Dermatology, The Rockefeller University, New York City, New York, United States of America ; Center for Clinical and Translational Science, The Rockefeller University, New York City, New York, United States of America ; Department of Dermatology, Mount Sinai School of Medicine, New York City, New York, United States of America.
Mayte Suárez-FariñasLaboratory for Investigative Dermatology, The Rockefeller University, New York City, New York, United States of America ; Center for Clinical and Translational Science, The Rockefeller University, New York City, New York, United States of America.
James G KruegerLaboratory for Investigative Dermatology, The Rockefeller University, New York City, New York, United States of America ; Center for Clinical and Translational Science, The Rockefeller University, New York City, New York, United States of America.
Rockefeller University · USIcahn School of Medicine at Mount Sinai · US

Funding

Weill Cornell/Rockefeller/Sloan-Kettering MST ProgramT32GM007739 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI HSU, KATHARINE C · 1985 to 2023
$51.1M
NIGMS NIH HHS T32 GM007739
6 · The paper itself

Abstract

backgroundIL-17 is the defining cytokine of the Th17, Tc17, and γδ T cell populations that plays a critical role in mediating inflammation and autoimmunity. Psoriasis vulgaris is an inflammatory skin disease mediated by Th1 and Th17 cytokines with relevant contributions of IFN-γ, TNF-α, and IL-17. Despite the pivotal role IL-17 plays in psoriasis, and in contrast to the other key mediators involved in the psoriasis cytokine cascade that are capable of inducing broad effects on keratinocytes, IL-17 was demonstrated to regulate the expression of a limited number of genes in monolayer keratinocytes cultured in vitro. METHODOLOGY/PRINCIPAL

findingsGiven the clinical efficacy of anti-IL-17 agents is associated with an impressive reduction in a large set of inflammatory genes, we sought a full-thickness skin model that more closely resemble in vivo epidermal architecture. Using a reconstructed human epidermis (RHE), IL-17 was able to upregulate 419 gene probes and downregulate 216 gene probes. As possible explanation for the increased gene induction in the RHE model is that C/CAAT-enhancer-binding proteins (C/EBP) -β, the transcription factor regulating IL-17-responsive genes, is expressed preferentially in differentiated keratinocytes. CONCLUSIONS/SIGNIFICANCE: The genes identified in IL-17-treated RHE are likely relevant to the IL-17 effects in psoriasis, since ixekizumab (anti-IL-17A agent) strongly suppressed the "RHE" genes in psoriasis patients treated in vivo with this IL-17 antagonist.

Indexed as

beta-DefensinsCCAAT-Enhancer-Binding Protein-betaEpidermal CellsEpidermisGene Expression ProfilingGene Expression RegulationHumansInterleukin-17KeratinocytesLipocalinsTissue Culture TechniquesTissue Engineeringbeta-DefensinsCCAAT-Enhancer-Binding Protein-betaCEBPB protein, humanDEFB4A protein, humanInterleukin-17Lipocalins

Identifiers

PMID24587313
PMCPMC3938679
OpenAlexW2020760332

What Socratic holds

Textmetadata
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 Socratic graph.