Evidence map›Paper›PMID 19632226›Full record

ArticleGastroenterology2009

High and low vitamin A therapies induce distinct FoxP3+ T-cell subsets and effectively control intestinal inflammation.

Seung G Kang, Chuanwu Wang, Satoshi Matsumoto, Chang H Kim

Open access · bronzeAbstract read
In one paragraph

Article in Gastroenterology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

46 citing papers in PubMed, 93 citations in OpenAlex.

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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

4 authors at 2 institutions in 2 countries.

Seung G KangDepartment of Comparative Pathobiology, Laboratory of Immunology and Hematopoiesis, Purdue Cancer Center, Purdue University, West Lafayette, Indiana 47907, USA.
Chuanwu Wang
Satoshi Matsumoto
Chang H Kim
Purdue University West Lafayette · USYakult Central Institute · JP

Funding

FoxP3+ T cells of mucosal tissuesR01AI074745 · NIAID · PURDUE UNIVERSITY · PI KIM, CHANG H · 2008 to 2012
$1.7M
Therapeutic delivery of FoxP3+ T cells to the intestineR01DK076616 · NIDDK · PURDUE UNIVERSITY · PI KIM, CHANG H · 2008 to 2012
$1.5M
NIAID NIH HHS 1R01AI074745NIAID NIH HHS R01 AI074745NIDDK NIH HHS 1R01DK076616NIDDK NIH HHS R01 DK076616
6 · The paper itself

Abstract

BACKGROUND &

aimsRetinoic acid plays a positive role in induction of FoxP3(+) regulatory T cells. Because retinoic acid is produced as a metabolite of vitamin A in the intestine and FoxP3(+) T cells regulate intestinal inflammation, we investigated the impact of vitamin A status on the regulatory T cells and inflammation in the intestine.

methodsThe SAMP1/YP model is a mouse model of Crohn's disease. We made vitamin A-deficient, vitamin A-excessive, and normal SAMP1/YP mice and assessed the intestinal inflammation. We also investigated the phenotype and function of FoxP3(+) T cells induced in different levels of vitamin A availability in regulation of intestinal inflammation in a T-cell-induced inflammation model in SCID mice.

resultsThe limited and excessive vitamin A conditions induced distinct FoxP3(+) T-cell subsets in vivo, and both ameliorated the intestinal inflammation in SAMP1/YP mice. The limited vitamin A condition greatly induced unusual CD103(+)CCR7(+) FoxP3(+) cells, while the high vitamin A condition induced CCR9(+)alpha4beta7(+) FoxP3(+) T cells in the intestine. Both FoxP3(+) T-cell populations, when transferred into mice with ongoing intestinal inflammation, were highly effective in reversing the inflammation. Blockade or lack of occupancy of RARalpha is a mechanism to induce highly suppressive CD103(+)CCR7(+) FoxP3(+) cells in both the thymus and periphery in limited vitamin A availability.

conclusionsOur results identify novel pathways of inducing highly suppressive FoxP3(+) regulatory T cells that can effectively control intestinal inflammation. The results have significant ramifications in treating inflammatory bowel diseases.

Indexed as

Adoptive TransferAnimalsAntigens, CDAnti-Inflammatory AgentsCell MovementCells, CulturedCoculture TechniquesCrohn DiseaseDisease Models, AnimalForkhead Transcription FactorsGastrointestinal AgentsImmunophenotypingIntegrin alpha ChainsIntestinesMiceMice, Inbred BALB Calpha E integrinsAntigens, CDAnti-Inflammatory AgentsCC chemokine receptor 9Ccr7 protein, mouseForkhead Transcription FactorsFoxp3 protein, mouseGastrointestinal AgentsIntegrin alpha ChainsRara protein, mouseReceptors, CCRReceptors, CCR7Receptors, Retinoic AcidRetinoic Acid Receptor alphaTretinoinVitamin A

Identifiers

PMID19632226
PMCPMC2757541
OpenAlexW2101875461

What OpenQuestion holds

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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.