Evidence map›Paper›PMID 27936495›Full record

ArticleClinical and experimental immunology2017

T-bet over-expression regulates aryl hydrocarbon receptor-mediated T helper type 17 differentiation through an interferon (IFN)γ-independent pathway.

M Yokosawa, Y Kondo, M Tahara, M Iizuka-Koga, S Segawa, S Kaneko, H Tsuboi, K Yoh, S Takahashi, I Matsumoto and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.3field-weighted citation impact, top 35% 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

5 citing papers in PubMed, 7 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

11 authors at 1 institution in 1 country.

M YokosawaDivision of Rheumatology, Department of Internal Medicine, University of Tsukuba, Tsukuba city, Ibaraki, Japan.
Y KondoDivision of Rheumatology, Department of Internal Medicine, University of Tsukuba, Tsukuba city, Ibaraki, Japan.
M TaharaDivision of Rheumatology, Department of Internal Medicine, University of Tsukuba, Tsukuba city, Ibaraki, Japan.
M Iizuka-KogaDivision of Rheumatology, Department of Internal Medicine, University of Tsukuba, Tsukuba city, Ibaraki, Japan.
S SegawaDivision of Rheumatology, Department of Internal Medicine, University of Tsukuba, Tsukuba city, Ibaraki, Japan.
S KanekoDivision of Rheumatology, Department of Internal Medicine, University of Tsukuba, Tsukuba city, Ibaraki, Japan.
H TsuboiDivision of Rheumatology, Department of Internal Medicine, University of Tsukuba, Tsukuba city, Ibaraki, Japan.
K YohDivision of Nephrology, Department of Medicine, University of Tsukuba, Tsukuba city, Ibaraki, Japan.
S TakahashiDepartment of Anatomy and Embryology, University of Tsukuba, Tsukuba city, Ibaraki, Japan.
I MatsumotoDivision of Rheumatology, Department of Internal Medicine, University of Tsukuba, Tsukuba city, Ibaraki, Japan.
T SumidaDivision of Rheumatology, Department of Internal Medicine, University of Tsukuba, Tsukuba city, Ibaraki, Japan.
University of Tsukuba · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Various transcription factors are also known to enhance or suppress T helper type 17 (Th17) differentiation. We have shown previously that the development of collagen-induced arthritis was suppressed in T-bet transgenic (T-bet Tg) mice, and T-bet seemed to suppress Th17 differentiation through an interferon (IFN)-γ-independent pathway, although the precise mechanism remains to be clarified. The present study was designed to investigate further the mechanisms involved in the regulation of Th17 differentiation by T-bet over-expression, and we found the new relationship between T-bet and aryl hydrocarbon receptor (AHR). Both T-bet Tg mice and IFN-γ

Indexed as

Cell DifferentiationGene ExpressionSignal TransductionAnimalsArthritis, ExperimentalCells, CulturedDisease Models, AnimalImmunomodulationImmunophenotypingInterferon-gammaInterleukin-6MiceMice, KnockoutMice, TransgenicModels, BiologicalReceptors, Aryl HydrocarbonInterferon-gammaInterleukin-6Receptors, Aryl HydrocarbonSTAT3 Transcription FactorT-bet Transcription FactorT-Box Domain ProteinsAHRIL-17T-bet over-expression

Identifiers

PMID27936495
PMCPMC5343350
OpenAlexW2620957046

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.