Evidence map›Paper›PMID 27554818›Full record

ArticleThe Journal of allergy and clinical immunology2017

IL-4 impairs wound healing potential in the skin by repressing fibronectin expression.

Ana P M Serezani, Gunseli Bozdogan, Sarita Sehra, Daniel Walsh, Purna Krishnamurthy, Elizabeth A Sierra Potchanant, Grzegorz Nalepa, Shreevrat Goenka, Matthew J Turner, Dan F Spandau and 1 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

41 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
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  3. Keratinocytes: pleiotropic orchestrators of cutaneous immunity and Inflammation - Emerging therapeutic paradigms in dermatological pathologies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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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

11 authors at 2 institutions in 1 country.

Ana P M SerezaniDepartment of Pediatrics, H.B. Wells Center for Pediatric Research and Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Ind.
Gunseli BozdoganDepartment of Pediatrics, H.B. Wells Center for Pediatric Research and Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Ind.
Sarita SehraDepartment of Pediatrics, H.B. Wells Center for Pediatric Research and Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Ind.
Daniel WalshDepartment of Pediatrics, H.B. Wells Center for Pediatric Research and Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Ind.
Purna KrishnamurthyDepartment of Pediatrics, H.B. Wells Center for Pediatric Research and Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Ind.
Elizabeth A Sierra PotchanantDepartment of Pediatrics, H.B. Wells Center for Pediatric Research and Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Ind; Division of Pediatric Hematology-Oncology Bone Marrow Failure Program, Indiana University School of Medicine, Indianapolis, Ind; Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, Ind.
Grzegorz NalepaDepartment of Pediatrics, H.B. Wells Center for Pediatric Research and Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Ind; Division of Pediatric Hematology-Oncology Bone Marrow Failure Program, Indiana University School of Medicine, Indianapolis, Ind; Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, Ind.
Shreevrat GoenkaDepartment of Pediatrics, H.B. Wells Center for Pediatric Research and Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Ind.
Matthew J TurnerDepartment of Dermatology, Indiana University School of Medicine, Indianapolis, Ind.
Dan F SpandauDepartment of Dermatology, Indiana University School of Medicine, Indianapolis, Ind.
Mark H KaplanDepartment of Pediatrics, H.B. Wells Center for Pediatric Research and Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Ind. Electronic address: mkaplan2@iupui.edu.
Indiana University School of MedicineIndiana University – Purdue University Indianapolis · US

Funding

BASIC SCIENCE STUDIES ON GENE THERAPY OF BLOOD DISEASEST32HL007910 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI Roland W. Herzog, Reuben Kapur · 1999 to 2026
$7.6M
Cytokine regulation of skin barrier functionR01AI095282 · NIAID · INDIANA UNIVERSITY INDIANAPOLIS · PI KAPLAN, MARK H · 2012 to 2022
$4.3M
Indiana Pediatric Scientist Award(IPSA)K12HD068371 · NICHD · INDIANA UNIVERSITY INDIANAPOLIS · PI CLAPP, DAVID W · 2013 to 2017
$1.9M
Postdoctoral Research Training in Pediatric Clinical PharmacologyT32HD069047 · NICHD · INDIANA UNIVERSITY INDIANAPOLIS · PI RENBARGER, JAMIE L · 2011 to 2020
$1.9M
Mechanisms of photocarcinogenesis in geriatric skinR01ES020866 · NIEHS · INDIANA UNIVERSITY INDIANAPOLIS · PI SPANDAU, DAN F, TRAVERS, JEFFREY B. · 2012 to 2016
$1.7M
CSRD VA IK2 CX001019NHLBI NIH HHS T32 HL007910NIAID NIH HHS R01 AI095282NICHD NIH HHS K12 HD068371NICHD NIH HHS T32 HD069047NIEHS NIH HHS R01 ES020866
6 · The paper itself

Abstract

backgroundAtopic dermatitis (AD) is characterized by intense pruritis and is a common childhood inflammatory disease. Many factors are known to affect AD development, including the pleiotropic cytokine IL-4. Yet little is known regarding the direct effects of IL-4 on keratinocyte function. OBJECTIVE AND

methodsIn this report RNA sequencing and functional assays were used to define the effect of the allergic environment on primary keratinocyte function and wound repair in mice.

resultsAcute or chronic stimulation by IL-4 modified expression of more than 1000 genes expressed in human keratinocytes that are involved in a broad spectrum of nonoverlapping functions. Among the IL-4-induced changes, repression of fibronectin critically impaired the human keratinocyte wound response. Moreover, in mouse models of spontaneous and induced AD-like lesions, there was delayed re-epithelialization. Importantly, topical treatment with fibronectin restored the epidermal repair response.

conclusionKeratinocyte gene expression is critically shaped by IL-4, altering cell fate decisions, which are likely important for the clinical manifestations and pathology of allergic skin disease.

Indexed as

AnimalsCells, CulturedFemaleFibronectinsGene Expression RegulationHumansInterleukin-4KeratinocytesMice, Inbred BALB CMice, Inbred C57BLMice, TransgenicSkinSTAT6 Transcription FactorTranscriptomeWound HealingFibronectinsInterleukin-4Stat6 protein, mouseSTAT6 Transcription Factoratopic dermatitisfibronectinIL-4KeratinocyteRNA sequencingwound healing

Identifiers

PMID27554818
PMCPMC5222746
OpenAlexW2514892365

What OpenQuestion holds

Textmetadata
LicenceTDM
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.