Evidence map›Paper›PMID 28617945›Full record

ArticleImmunology2017

microRNA cluster 106a~363 is involved in T helper 17 cell differentiation.

Marc Kästle, Sabine Bartel, Kerstin Geillinger-Kästle, Martin Irmler, Johannes Beckers, Bernhard Ryffel, Oliver Eickelberg, Susanne Krauss-Etschmann

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 71 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

8 authors at 2 institutions in 1 country.

Marc KästleComprehensive Pneumology Centre, Helmholtz Zentrum München, University Hospital of the Ludwig Maximilians University, Member of the German Centre for Lung Research, Munich, Germany.
Sabine BartelComprehensive Pneumology Centre, Helmholtz Zentrum München, University Hospital of the Ludwig Maximilians University, Member of the German Centre for Lung Research, Munich, Germany.ORCID 0000-0002-9163-795X
Kerstin Geillinger-KästleDepartment of Biochemistry, ZIEL Research Centre of Nutrition and Food Sciences, Technical University Munich, Freising, Germany.
Martin IrmlerInstitute of Experimental Genetics, Helmholtz Zentrum Munich, Neuherberg, Germany.
Johannes BeckersInstitute of Experimental Genetics, Helmholtz Zentrum Munich, Neuherberg, Germany.
Bernhard RyffelMolecular and Experimental Immunology and Neurogenetics, CNRS, University of Orléans, Orléans, Germany.
Oliver EickelbergComprehensive Pneumology Centre, Helmholtz Zentrum München, University Hospital of the Ludwig Maximilians University, Member of the German Centre for Lung Research, Munich, Germany.
Susanne Krauss-EtschmannComprehensive Pneumology Centre, Helmholtz Zentrum München, University Hospital of the Ludwig Maximilians University, Member of the German Centre for Lung Research, Munich, Germany.ORCID 0000-0001-5945-5702
Helmholtz Zentrum München · DELeibniz-Institute for Food Systems Biology at the Technical University of Munich · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T-helper cell type 17 (Th17) mediated inflammation is associated with various diseases including autoimmune encephalitis, inflammatory bowel disease and lung diseases such as chronic obstructive pulmonary disease and asthma. Differentiation into distinct T helper subtypes needs to be tightly regulated to ensure an immunological balance. As microRNAs (miRNAs) are critical regulators of signalling pathways, we aimed to identify specific miRNAs implicated in controlling Th17 differentiation. We were able to create a regulatory network model of murine T helper cell differentiation by combining Affymetrix mRNA and miRNA arrays and in silico analysis. In this model, the miR-212~132 and miR-182~183 clusters were significantly up-regulated upon Th17 differentiation, whereas the entire miR-106~363 cluster was down-regulated and predicted to target well-known Th17 cell differentiation pathways. In vitro transfection of miR-18b, miR-106a and miR-363-3p into primary murine Cd4

Indexed as

Cell DifferentiationAnimalsCells, CulturedFemaleGene Expression ProfilingGene Expression RegulationGene Regulatory NetworksInterleukin-17Mice, Inbred BALB CMicroRNAsNuclear Receptor Subfamily 1, Group F, Member 1Nuclear Receptor Subfamily 1, Group F, Member 3Oligonucleotide Array Sequence AnalysisPhenotypeSignal TransductionTh17 CellsIl17a protein, mouseInterleukin-17microRNA 363, mouseMicroRNAsMirn106 microRNA, mouseMIRN18 microRNA, mouseNfat5 protein, mouseNuclear Receptor Subfamily 1, Group F, Member 1Nuclear Receptor Subfamily 1, Group F, Member 3Rora protein, mouseRorc protein, mouseTranscription FactorsmicroRNAmiR-106amiR-18bmiR-363a-3pnuclear factor of activated T cells 5retinoid-related orphan receptor αretinoid-related orphan receptor γtT helper cell differentiationT helper type 17

Identifiers

PMID28617945
PMCPMC5629441
OpenAlexW2625737972

What OpenQuestion holds

Textmetadata
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.