Evidence map›Paper›PMID 20081874›Full record

ArticleCellular & molecular immunology2010

TGF-beta1 gene-modified, immature dendritic cells delay the development of inflammatory bowel disease by inducing CD4(+)Foxp3(+) regulatory T cells.

Zhijian Cai, Wei Zhang, Min Li, Yinpu Yue, Fei Yang, Lei Yu, Xuetao Cao, Jianli Wang

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

18 citing papers in PubMed, 36 citations in OpenAlex.

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  12. Association among genetic predisposition, gut microbiota, and host immune response in the etiopathogenesis of inflammatory bowel disease.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2014
    Review
  13. Serum adipokines in inflammatory bowel disease.World journal of gastroenterology · 2014
    Article
  14. Article
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  18. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Zhijian CaiInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou, China.
Wei Zhang
Min Li
Yinpu Yue
Fei Yang
Lei Yu
Xuetao Cao
Jianli Wang
Zhejiang University · CNSecond Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory bowel disease (IBD) is caused by an uncontrolled immune response in the intestinal lumen, leading to inflammation in genetically predisposed individuals. Immunotherapy may be a promising approach to the treatment of IBD. Here, we show that transforming growth factor-beta1 (TGF-beta1) gene-modified immature dendritic cells (imDCs) could enhance the inhibitory function of imDCs and delay the progress of IBD induced by dextran sodium sulfate in mice. The results of fluorescence-activated cell sorter (FACS) demonstrated that this protective effect is mediated partially by inducing CD4(+)Foxp3(+) regulatory T cells (Tregs) in mesentery lymph nodes to control inflammation. In vitro experiments also supported this hypothesis. In conclusion, we provide evidence that TGF-beta1-modified bone marrow-derived imDCs may have a therapeutic effect to IBD.

Indexed as

Cell DifferentiationAnimalsCell MovementCells, CulturedDendritic CellsFemaleForkhead Transcription FactorsInflammatory Bowel DiseasesMiceMice, Inbred BALB CMice, Inbred C57BLT-Lymphocytes, RegulatoryTransforming Growth Factor beta1Forkhead Transcription FactorsFoxp3 protein, mouseTransforming Growth Factor beta1

Identifiers

PMID20081874
PMCPMC4003258
OpenAlexW4232019095

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.