Evidence map›Paper›PMID 23616302›Full record

ArticleEuropean journal of immunology2013

Transgenic expression of survivin compensates for OX40-deficiency in driving Th2 development and allergic inflammation.

Fengyang Lei, Jianyong Song, Rizwanul Haque, Xiaofang Xiong, Deyu Fang, Yuzhang Wu, Susanne M A Lens, Michael Croft, Jianxun Song

Open access · greenAbstract read
In one paragraph

Article in European journal of immunology, 2013. 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
0.9field-weighted citation impact, top 27% 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, 15 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Stem Cell-Derived Regulatory T Cells for Therapeutic Use in Arthritis.Autoimmune and infectious diseases : open access · 2016
    Article
  8. Article
  9. Article
  10. Article
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

9 authors at 4 institutions in 3 countries.

Fengyang LeiDepartment of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, PA, USA.
Jianyong Song
Rizwanul Haque
Xiaofang Xiong
Deyu Fang
Yuzhang Wu
Susanne M A Lens
Michael Croft
Jianxun Song
Pennsylvania State University · USNorthwestern University · USArmy Medical University · CNLa Jolla Institute for Immunology · US

Funding

TRM and airway inflammation and remodelingU19AI070535 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROIDE, DAVID H · 2006 to 2025
$34.2M
The roles of Sirt1, a deacetylase, in immune tolerance and autoimmunityR01AI079056 · NIAID · UNIVERSITY OF MISSOURI-COLUMBIA · PI FANG, DEYU · 2008 to 2017
$3.3M
Impact of Highly Active T Lymphocytes from Induced Pluripotent Stem CellsK18CA151798 · NCI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI SONG, JIANXUN JIM · 2011 to 2012
$234k
NCI NIH HHS K18 CA151798NCI NIH HHS K18CA151798NIAID NIH HHS R01 AI079056NIAID NIH HHS R01AI079056NIAID NIH HHS U19 AI070535
6 · The paper itself

Abstract

Survivin, an inhibitor of apoptosis family molecule, has been proposed as a crucial intermediate in the signaling pathways leading to T-cell development, proliferation, and expansion. However, the importance of survivin to T-cell-driven inflammatory responses has not been demonstrated. Here, we show that survivin transgenic mice exhibit an increased antigen-driven Th2 lung inflammation and that constitutive expression of survivin reversed the defective lung inflammation even in the absence of OX40 costimulation. We found that OX40-deficient mice were compromised in generating Th2 cells, airway eosinophilia, and IgE responses. In contrast, OX40-deficient/survivin transgenic mice generated normal Th2 responses and exhibited strong lung inflammation. These results suggest that OX40 costimulation crucially engages survivin during antigen-mediated Th2 responses. These findings also promote the notion that OX40 costimulation regulates allergic responses or lung inflammation by targeting survivin thereby enhancing T-cell proliferation and resulting in more differentiated Th2 cells in the allergic inflammatory response.

Indexed as

AnimalsCell DifferentiationHypersensitivityInhibitor of Apoptosis ProteinsLymphocyte ActivationMiceMice, Inbred C57BLMice, TransgenicPneumoniaReceptors, OX40Repressor ProteinsSurvivinTh2 CellsBirc5 protein, mouseInhibitor of Apoptosis ProteinsReceptors, OX40Repressor ProteinsSurvivinTnfrsf4 protein, mouseCostimulationLung inflammationMurine modelSurvivinTh2 cells

Identifiers

PMID23616302
PMCPMC3876962
OpenAlexW1563646381

What OpenQuestion holds

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LicenceTDM
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.