Evidence map›Paper›PMID 27286791›Full record

ArticleJournal of leukocyte biology2016

IRF2BP2 transcriptional repressor restrains naive CD4 T cell activation and clonal expansion induced by TCR triggering.

Cristiane Sécca, Douglas V Faget, Steffi C Hanschke, Mayra S Carneiro, Martin H Bonamino, Patricia S de-Araujo-Souza, João P B Viola

Open access · bronzeAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2016. 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
0.5field-weighted citation impact, top 34% 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, 23 citations in OpenAlex.

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  11. Pharmaceuticals (Basel, Switzerland) · 2021
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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

7 authors at 1 institution in 1 country.

Cristiane SéccaProgram of Cellular Biology, Brazilian National Cancer Institute, Rio de Janeiro, RJ, Brazil.
Douglas V FagetProgram of Cellular Biology, Brazilian National Cancer Institute, Rio de Janeiro, RJ, Brazil.
Steffi C HanschkeProgram of Cellular Biology, Brazilian National Cancer Institute, Rio de Janeiro, RJ, Brazil.
Mayra S CarneiroProgram of Molecular Carcinogenesis, Brazilian National Cancer Institute, Rio de Janeiro, RJ, Brazil.
Martin H BonaminoProgram of Molecular Carcinogenesis, Brazilian National Cancer Institute, Rio de Janeiro, RJ, Brazil.
Patricia S de-Araujo-SouzaProgram of Cellular Biology, Brazilian National Cancer Institute, Rio de Janeiro, RJ, Brazil.
João P B ViolaProgram of Cellular Biology, Brazilian National Cancer Institute, Rio de Janeiro, RJ, Brazil; jpviola@inca.gov.br.
Instituto Nacional do Câncer · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD4 T cell activation and differentiation mechanisms constitute a complex and intricate signaling network involving several regulatory proteins. IRF2BP2 is a transcriptional repressor that is involved in gene-expression regulation in very diverse biologic contexts. Information regarding the IRF2BP2 regulatory function in CD4 T lymphocytes is very limited and suggests a role for this protein in repressing the expression of different cytokine genes. Here, we showed that Irf2bp2 gene expression was decreased in CD4 T cells upon activation. To investigate the possible regulatory roles for IRF2BP2 in CD4 T cell functions, this protein was ectopically expressed in murine primary-activated CD4 T lymphocytes through retroviral transduction. Interestingly, ectopic expression of IRF2BP2 led to a reduction in CD25 expression and STAT5 phosphorylation, along with an impaired proliferative capacity. The CD69 expression was also diminished in IRF2BP2-overexpressing cells, whereas CD44 and CD62L levels were not altered. In vivo, transferred, IRF2BP2-overexpressing, transduced cells displayed an impaired expansion capacity compared with controls. Furthermore, overexpression of IRF2BP2 in differentiated Th cells resulted in slightly reduced IL-4 and pro-TGF-β production in Th2 and iT

Indexed as

AnimalsAntigens, CDAntigens, Differentiation, T-LymphocyteApoptosisCD4-Positive T-LymphocytesCD69 AntigensCells, CulturedCytokinesFemaleGene Expression RegulationHumansInterleukin-2 Receptor alpha SubunitLectins, C-TypeLymphocyte ActivationMaleMiceAntigens, CDAntigens, Differentiation, T-LymphocyteCD69 AntigensCytokinesIl2ra protein, mouseInterleukin-2 Receptor alpha SubunitIRF2BP2 protein, mouseLectins, C-TypeReceptors, Antigen, T-CellRecombinant Fusion ProteinsRNA, MessengerSTAT5 Transcription FactorTranscription FactorsCD25lymphocyte proliferationsurvival

Identifiers

PMID27286791
PMCPMC6608065
OpenAlexW2419650898

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.