Evidence map›Paper›PMID 28685820›Full record

ArticleImmunology2017

PI3K-Akt pathway enhances the differentiation of interleukin-27-induced type 1 regulatory T cells.

Niken Adiba Nadya, Hiroyuki Tezuka, Toshiaki Ohteki, Satoshi Matsuda, Miyuki Azuma, Shigenori Nagai

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 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. AIM2 and Psoriasis.Frontiers in immunology · 2023
    Review
  6. Review
  7. Article
  8. Article
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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

6 authors at 2 institutions in 1 country.

Niken Adiba NadyaDepartment of Molecular Immunology, Graduate School, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan.ORCID 0000-0003-4083-0538
Hiroyuki TezukaLife Science Tokyo Advanced Research Centre, School of Pharmacy and Pharmaceutical Sciences, Hoshi University, Shinagawa-ku, Tokyo, Japan.
Toshiaki OhtekiDepartment of Biodefence, Medical Research Institute, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan.
Satoshi MatsudaDepartment of Cell Signalling, Institute of Biomedical Science, Kansai Medical University, Moriguchi, Osaka, Japan.
Miyuki AzumaDepartment of Molecular Immunology, Graduate School, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan.ORCID 0000-0002-3529-4585
Shigenori NagaiDepartment of Molecular Immunology, Graduate School, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan.
Tokyo Medical and Dental University · JPKansai Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin 27 (IL-27) has been identified as a potent cytokine in the differentiation of type 1 regulatory T (Tr1) cells through interactions with several key elements, including transcription factors such as aryl hydrocarbon receptor and IL-21. Autocrine production of IL-21 is known to be important for maintaining IL-10 expression by Tr1 cells. Although previous studies have shown that the phosphoinositide 3-kinase (PI3K) -Akt axis contributes to the differentiation of helper T-cell subsets, the role of the PI3K pathway on Tr1 cell differentiation remains to be elucidated. Here, we demonstrate that suppression of the PI3K-Akt pathway results in impairment of IL-27-induced Tr1 (IL-27-Tr1) cell differentiation in vitro and in vivo. Furthermore, this suppression down-regulates IL-21 receptor expression by Tr1 cells, followed by suppression of IL-10 expression by IL-27-Tr1 cells. These results suggest that the PI3K pathway enhances IL-10 expression by IL-27-Tr1 cells through up-regulation of IL-21 receptors.

Indexed as

AnimalsCell DifferentiationCells, CulturedFemaleForkhead Box Protein O1Forkhead Transcription FactorsGenotypeInterleukin-10Interleukin-21 Receptor alpha SubunitInterleukin-27Mice, Inbred BALB CMice, Inbred C57BLMice, TransgenicPhenotypePhosphatidylinositol 3-KinasePhosphoinositide-3 Kinase InhibitorsForkhead Box Protein O1Forkhead Transcription FactorsFoxo1 protein, mouseFoxp3 protein, mouseIL10 protein, mouseIl21r protein, mouseInterleukin-10Interleukin-21 Receptor alpha SubunitInterleukin-27Phosphatidylinositol 3-KinasePhosphoinositide-3 Kinase InhibitorsProtein Kinase InhibitorsProto-Oncogene Proteins c-aktinterleukin-21 receptorinterleukin-27phosphoinositide 3-kinasetype 1 regulatory T cells

Identifiers

PMID28685820
PMCPMC5629445
OpenAlexW2731405111

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.