Evidence map›Paper›PMID 27284976›Full record

ArticlePloS one2016

The Transcriptional Repressor Gfi1 Plays a Critical Role in the Development of NKT1- and NKT2-Type iNKT Cells.

Toshiaki Yasuoka, Makoto Kuwahara, Takeshi Yamada, Saho Maruyama, Junpei Suzuki, Masaru Taniguchi, Masaki Yasukawa, Masakatsu Yamashita

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 37% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Review
  3. Mouse Models and Tools for theFrontiers in immunology · 2019
    Review
  4. Review
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 3 institutions in 1 country.

Toshiaki YasuokaDepartment of Obstetrics and Gynecology, Graduate School of Medicine, Ehime University, Shitsukawa, Toon, Ehime, Japan.
Makoto KuwaharaDepartment of Immunology, Graduate School of Medicine, Ehime University, Shitsukawa, Toon, Ehime, Japan.
Takeshi YamadaDepartment of Infection and Host Defenses, Graduate School of Medicine, Ehime University, Shitsukawa, Toon, Ehime, Japan.
Saho MaruyamaDepartment of Immunology, Graduate School of Medicine, Ehime University, Shitsukawa, Toon, Ehime, Japan.
Junpei SuzukiTranslational Research Center, Ehime University Hospital, Shitsukawa, Toon, Ehime, Japan.
Masaru TaniguchiLaboratory of Immune Regulation, RIKEN Center for Integrative Medical Sciences, 1-7-22 suehiro-cho, Tsurumi-ku, Yokohama, Japan.
Masaki YasukawaDepartment of Hematology, Clinical Immunology and Infectious Diseases, Graduate School of Medicine, Ehime University, Shitsukawa, Toon, Ehime, Japan.
Masakatsu YamashitaDepartment of Immunology, Graduate School of Medicine, Ehime University, Shitsukawa, Toon, Ehime, Japan.
Ehime University · JPEhime University Hospital · JPRIKEN Center for Integrative Medical Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gfi1 plays an important role in the development and maintenance of many hematopoietic linage cells. However, the impact of Gfi1-deficiency on the iNKT cell differentiation remains unclear. We herein demonstrate a critical role of Gfi1 in regulating the development of iNKT cell subsets. In the thymus of T cell-specific Gfi1-deficient mice, iNKT cells normally developed up to stage 2, while the number of stage 3 NK1.1pos iNKT cells was significantly reduced. Furthermore, CD4pos iNKT cells were selectively reduced in the peripheral organs of T cell-specific Gfi1-deficient mice. The α-GalCer-dependent production of IFN-γand Th2 cytokines, but not IL-17A, was severely reduced in T cell-specific Gfi1-deficient mice. In addition, a reduction of the α-GalCer-induced anti-tumor activity was observed in Gfi1-deficient mice. These findings demonstrate the important role of Gfi1 in regulating the development and function of NKT1- and NKT2-type iNKT cell subsets.

Indexed as

AnimalsAntigens, LyCD4 AntigensCell DifferentiationCytokinesDNA-Binding ProteinsGalactosylceramidesGene DeletionGene Knock-In TechniquesInterferon-gammaLung NeoplasmsMelanoma, ExperimentalMiceNatural Killer T-CellsNK Cell Lectin-Like Receptor Subfamily BTranscription Factorsalpha-galactosylceramideAntigens, LyCD4 AntigensCytokinesDNA-Binding ProteinsGalactosylceramidesGfi1 protein, mouseInterferon-gammaKlrb1c protein, mouseNK Cell Lectin-Like Receptor Subfamily BTranscription Factors

Identifiers

PMID27284976
PMCPMC4902269
OpenAlexW2413300743

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.