Evidence map›Paper›PMID 21919915›Full record

ArticleAllergy2012

Increased expression of IRF4 and ETS1 in CD4+ cells from patients with intermittent allergic rhinitis.

S Bruhn, F Barrenäs, R Mobini, B A Andersson, S Chavali, B S Egan, E Hovig, G K Sandve, M A Langston, G Rogers and 2 more

Abstract read
In one paragraph

Article in Allergy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed, 28 citations in OpenAlex.

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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

12 authors at 8 institutions in 4 countries.

S BruhnThe Centre for Individualized Medication, Linköping University Hospital, Linköping, Sweden.
F Barrenäs
R Mobini
B A Andersson
S Chavali
B S Egan
E Hovig
G K Sandve
M A Langston
G Rogers
H Wang
M Benson
Linköping University Hospital · SEUniversity of Tennessee at Knoxville · USDrottning Silvias barn- och ungdomssjukhus · SEMRC Laboratory of Molecular Biology · GBOslo University Hospital · NOPathway Genomics (United States) · USSahlgrenska University Hospital · SEUniversity of Oslo · NO

Funding

INIA: Stress, Anxiety of Alcohol AbuseU01AA013641 · NIAAA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI GRANT, KATHLEEN A · 2002 to 2015
$8.8M
Bioinfomatics for Mouse Phenotype AnalysisP01DA015027 · NIDA · UNIVERSITY OF TENNESSEE KNOXVILLE · PI LANGSTON, MICHAEL ALLEN · 2002 to 2004
$1.8M
INIA: Informatics CoreU01AA013512 · NIAAA · UNIVERSITY OF TENNESSEE KNOXVILLE · PI LANGSTON, MICHAEL ALLEN · 2002 to 2006
$1.5M
Medical Research Council MC_U105185859NIAAA NIH HHS U01 AA013512NIAAA NIH HHS U01-AA-013512NIAAA NIH HHS U01 AA013641NIAAA NIH HHS U01-AA-013641-04NIDA NIH HHS P01 DA015027NIDA NIH HHS P01-DA-015027-01NIMH NIH HHS R01-MH-074460-01
6 · The paper itself

Abstract

backgroundThe transcription factor (TF) IRF4 is involved in the regulation of Th1, Th2, Th9, and Th17 cells, and animal studies have indicated an important role in allergy. However, IRF4 and its target genes have not been examined in human allergy.

methodsIRF4 and its target genes were examined in allergen-challenged CD4(+) cells from patients with IAR, using combined gene expression microarrays and chromatin immunoprecipitation chips (ChIP-chips), computational target prediction, and RNAi knockdowns.

resultsIRF4 increased in allergen-challenged CD4(+) cells from patients with IAR, and functional studies supported its role in Th2 cell activation. IRF4 ChIP-chip showed that IRF4 regulated a large number of genes relevant to Th cell differentiation. However, neither Th1 nor Th2 cytokines were the direct targets of IRF4. To examine whether IRF4 induced Th2 cytokines via one or more downstream TFs, we combined gene expression microarrays, ChIP-chips, and computational target prediction and found a putative intermediary TF, namely ETS1 in allergen-challenged CD4(+) cells from allergic patients. ETS1 increased significantly in allergen-challenged CD4(+) cells from patients compared to controls. Gene expression microarrays before and after ETS1 RNAi knockdown showed that ETS1 induced Th2 cytokines as well as disease-related pathways.

conclusionsIncreased expression of IRF4 in allergen-challenged CD4(+) cells from patients with intermittent allergic rhinitis leads to activation of a complex transcriptional program, including Th2 cytokines.

Indexed as

CD4-Positive T-LymphocytesCell DifferentiationCell SeparationChromatin ImmunoprecipitationGene Expression ProfilingGene Expression RegulationGene Knockdown TechniquesHumansInterferon Regulatory Factor-4Interferon Regulatory FactorsLymphocyte ActivationOligonucleotide Array Sequence AnalysisProto-Oncogene Protein c-ets-1Rhinitis, Allergic, SeasonalRNA, Small InterferingTh2 CellsETS1 protein, humanInterferon Regulatory Factor-4Interferon Regulatory FactorsProto-Oncogene Protein c-ets-1RNA, Small Interfering

Identifiers

PMID21919915
PMCPMC3237963
OpenAlexW2147235412

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.