Evidence map›Paper›PMID 26129652›Full record

ArticleMucosal immunology2016

Generation and transcriptional programming of intestinal dendritic cells: essential role of retinoic acid.

R Zeng, M Bscheider, K Lahl, M Lee, E C Butcher

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

53 citing papers in PubMed, 69 citations in OpenAlex.

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  18. A novelDiscovery immunology · 2023
    Article
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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

5 authors at 2 institutions in 3 countries.

R ZengLaboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University School of Medicine, Stanford, California, USA.
M BscheiderLaboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University School of Medicine, Stanford, California, USA.
K LahlLaboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University School of Medicine, Stanford, California, USA.
M LeeLaboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University School of Medicine, Stanford, California, USA.
E C ButcherLaboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University School of Medicine, Stanford, California, USA.
VA Palo Alto Health Care System · USSwedish Veterinary Agency · SE

Funding

Intestinal Lymphocyte TraffickingR37AI047822 · NIAID · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI BUTCHER, EUGENE C · 2011 to 2020
$3.5M
Novel Mucosa-homing Dendritic Cell: Development, Trafficking and FunctionR01AI093981 · NIAID · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI BUTCHER, EUGENE C · 2012 to 2016
$1.8M
NIAID NIH HHS R01 AI093981NIAID NIH HHS R01AI093981NIAID NIH HHS R37 AI047822
6 · The paper itself

Abstract

The vitamin A metabolite retinoic acid (RA) regulates adaptive immunity in the intestines, with well-characterized effects on IgA responses, Treg induction, and gut trafficking of T- and B-effector cells. It also controls the generation of conventional dendritic cell (cDC) precursors in the bone marrow and regulates cDC subset representation, but its roles in the specialization of intestinal cDC subsets are understudied. Here we show that RA acts cell intrinsically in developing gut-tropic pre-mucosal dendritic cell (pre-μDC) to effect the differentiation and drive the specialization of intestinal CD103(+)CD11b(-) (cDC1) and of CD103(+)CD11b(+) (cDC2). Systemic deficiency or DC-restricted antagonism of RA signaling resulted in altered phenotypes of intestinal cDC1 and cDC2, and reduced numbers of cDC2. Effects of dietary deficiency were most apparent in the proximal small intestine and were rapidly reversed by reintroducing vitamin A. In cultures of pre-μDC with Flt3L and granulocyte-macrophage colony-stimulating factor (GM-CSF), RA induced cDC with characteristic phenotypes of intestinal cDC1 and cDC2 by controlling subset-defining cell surface receptors, regulating subset-specific transcriptional programs, and suppressing proinflammatory nuclear factor-κB-dependent gene expression. Thus, RA is required for transcriptional programming and maturation of intestinal cDC, and with GM-CSF and Flt3L provides a minimal environment for in vitro generation of intestinal cDC1- and cDC2-like cDC from specialized precursors.

Indexed as

AnimalsAntigens, CDBone Marrow CellsCD11b AntigenCell LineageDendritic CellsGene Expression RegulationGranulocyte-Macrophage Colony-Stimulating FactorIntegrin alpha ChainsIntestinesMembrane ProteinsMiceMice, Inbred BALB CMice, Inbred C57BLPhenotypeSignal Transductionalpha E integrinsAntigens, CDCD11b Antigenflt3 ligand proteinGranulocyte-Macrophage Colony-Stimulating FactorIntegrin alpha ChainsMembrane ProteinsTretinoin

Identifiers

PMID26129652
PMCPMC4698111
OpenAlexW749232915

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.