Evidence map›Paper›PMID 23915137›Full record

ArticleBMC genomics2013

Dissecting the psoriasis transcriptome: inflammatory- and cytokine-driven gene expression in lesions from 163 patients.

William R Swindell, Andrew Johnston, John J Voorhees, James T Elder, Johann E Gudjonsson

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 2 pooled it
5.7field-weighted citation impact, top 3% 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

75 citing papers in PubMed, 2 syntheses or guidelines pooled it, 132 citations in OpenAlex.

  1. Pooled it
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  12. The Immunology of Psoriasis-Current Concepts in Pathogenesis.Clinical reviews in allergy & immunology · 2024
    Review
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15 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

5 authors at 1 institution in 1 country.

William R SwindellDepartment of Dermatology, University of Michigan School of Medicine, Ann Arbor, MI 48109-2200, USA. wswindel@umich.edu
Andrew Johnston
John J Voorhees
James T Elder
Johann E Gudjonsson
University of Michigan–Ann Arbor · US

Funding

Combined Analysis of Gene Expression and DNA Variation in PsoriasisR01AR054966 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ELDER, JAMES TILFORD · 2007 to 2011
$3.2M
Functional Genomics of PsoriasisR01AR065183 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ELDER, JAMES TILFORD · 2013 to 2016
$1.7M
Role of the Psoriasis Associated IL23R Risk Variants on Th17 Biology and FunctionK08AR060802 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GUDJONSSON, JOHANN ELI · 2011 to 2015
$636k
NIAMS NIH HHS K08 AR060802NIAMS NIH HHS NIH K08 AR060802NIAMS NIH HHS R01 AR054966NIAMS NIH HHS R01 AR065183
6 · The paper itself

Abstract

backgroundPsoriasis lesions are characterized by large-scale shifts in gene expression. Mechanisms that underlie differentially expressed genes (DEGs), however, are not completely understood. We analyzed existing datasets to evaluate genome-wide expression in lesions from 163 psoriasis patients. Our aims were to identify mechanisms that drive differential expression and to characterize heterogeneity among lesions in this large sample.

resultsWe identified 1233 psoriasis-increased DEGs and 977 psoriasis-decreased DEGs. Increased DEGs were attributed to keratinocyte activity (56%) and infiltration of lesions by T-cells (14%) and macrophages (11%). Decreased DEGs, in contrast, were associated with adipose tissue (63%), epidermis (14%) and dermis (4%). KC/epidermis DEGs were enriched for genes induced by IL-1, IL-17A and IL-20 family cytokines, and were also disproportionately associated with AP-1 binding sites. Among all patients, 50% exhibited a heightened inflammatory signature, with increased expression of genes expressed by T-cells, monocytes and dendritic cells. 66% of patients displayed an IFN-γ-strong signature, with increased expression of genes induced by IFN-γ in addition to several other cytokines (e.g., IL-1, IL-17A and TNF). We show that such differences in gene expression can be used to differentiate between etanercept responders and non-responders.

conclusionsPsoriasis DEGs are partly explained by shifts in the cellular composition of psoriasis lesions. Epidermal DEGs, however, may be driven by the activity of AP-1 and cellular responses to IL-1, IL-17A and IL-20 family cytokines. Among patients, we uncovered a range of inflammatory- and cytokine-associated gene expression patterns. Such patterns may provide biomarkers for predicting individual responses to biologic therapy.

Indexed as

Gene Expression ProfilingBinding SitesCytokinesDermisEpidermisEtanerceptGenomicsHumansImmunoglobulin GInflammationKeratinocytesOligonucleotide Array Sequence AnalysisOrgan SpecificityProteasome Endopeptidase ComplexPsoriasisReceptors, Tumor Necrosis FactorCytokinesEtanerceptImmunoglobulin GProteasome Endopeptidase ComplexReceptors, Tumor Necrosis FactorTranscription Factor AP-1Tumor Necrosis Factor-alpha

Identifiers

PMID23915137
PMCPMC3751090
OpenAlexW2082280403

What OpenQuestion 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 OpenQuestion graph.