Evidence map›Paper›PMID 19941313›Full record

ArticleEuropean journal of immunology2010

DC expressing transgene Foxp3 are regulatory APC.

Michael W Lipscomb, Jennifer L Taylor, Cristina J Goldbach, Simon C Watkins, Amy K Wesa, Walter J Storkus

Open access · bronzeAbstract read
In one paragraph

Article in European journal of immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Elevated Foxp3Frontiers in immunology · 2022
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. FoxP3 Expression in Macrophages, Cancer, and B Cells-Is It Real?Clinical reviews in allergy & immunology · 2017
    Review
  9. Effects of Foxp3 gene modified dendritic cells on mouse corneal allograft rejection.International journal of clinical and experimental medicine · 2015
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Michael W LipscombDepartment of Dermatology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Jennifer L Taylor
Cristina J Goldbach
Simon C Watkins
Amy K Wesa
Walter J Storkus
University of Pittsburgh · US

Funding

University of Pittsburgh Clinical and Translational Science InstituteUL1TR000005 · NCATS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REIS, STEVEN E · 2012 to 2015
$50.8M
Training in Cellular & Molecular Mechanisms of Tumor RejectionT32CA082084 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Robert J Binder, Dario AA Vignali · 1999 to 2026
$9.2M
VECTOR COREP01CA100327 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI STORKUS, WALTER J. · 2005 to 2009
$4.5M
NCATS NIH HHS UL1 TR000005NCI NIH HHS 5T32CA082084-08NCI NIH HHS P01 CA100327NCI NIH HHS T32 CA082084
6 · The paper itself

Abstract

Tolerogenic DC and suppressive Foxp3(+) Treg play important roles in preventing autoimmunity and allograft rejection. We report that (adenovirus mediated) ectopic expression of Foxp3 in human DC (i.e. DC.Foxp3) yields an APC that severely limits T-cell proliferation and type-1 immune responses from the naïve, but not memory, pool of responder T cells in vitro. In marked contrast, the frequencies of type-2 and Treg responses were dramatically increased after stimulation of naïve T cells with DC.Foxp3 versus control DC. DC.Foxp3-induced CD4(+)CD25(+) Treg cells potently suppressed the proliferation of, and IFN-gamma production from, CD4(+) and CD8(+) responder T cells. Notably, the immunosuppressive biology of DC.Foxp3 was effectively normalized by addition of 1-methyl-tryptophan or neutralizing anti-TGF-beta1 Ab during the period of T-cell priming. These data suggest the potential utility of regulatory DC.Foxp3 and/or DC.Foxp3-induced CD4(+)CD25(+) Treg as translational agents for the amelioration or prevention of pathology in the setting of allograft transplantation and/or autoimmunity.

Indexed as

Antibodies, NeutralizingAntigen-Presenting CellsBridged Bicyclo Compounds, HeterocyclicCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell ProliferationCells, CulturedCell SurvivalCoculture TechniquesCytokinesDendritic CellsFlow CytometryForkhead Transcription FactorsGene ExpressionHumansIndoleamine-Pyrrole 2,3,-Dioxygenase1-methyl-3-oxo-7-oxabicyclo(2.2.1)hept-5-ene-2-carboxylic acid methyl esterAntibodies, NeutralizingBridged Bicyclo Compounds, HeterocyclicCytokinesForkhead Transcription FactorsFOXP3 protein, humanIndoleamine-Pyrrole 2,3,-DioxygenaseInterferon-gammaInterleukin-2 Receptor alpha SubunitTransforming Growth Factor beta1

Identifiers

PMID19941313
PMCPMC3023581
OpenAlexW2143105903

What OpenQuestion holds

Textmetadata
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.