Evidence map›Paper›PMID 27027442›Full record

ArticleOncotarget2016

IL-10 control of CD11c+ myeloid cells is essential to maintain immune homeostasis in the small and large intestine.

Mathilde J H Girard-Madoux, Juliane L Ober-Blöbaum, Léa M M Costes, Junda M Kel, Dicky J Lindenbergh-Kortleve, Inge Brouwers-Haspels, Astrid P Heikema, Janneke N Samsom, Björn E Clausen

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

25 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
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  6. Antibiotic-induced depletion ofFrontiers in cellular and infection microbiology · 2022
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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

9 authors at 2 institutions in 2 countries.

Mathilde J H Girard-MadouxDepartment of Immunology, Erasmus MC, University Medical Center, 3015 GE Rotterdam, Netherlands.
Juliane L Ober-BlöbaumDepartment of Immunology, Erasmus MC, University Medical Center, 3015 GE Rotterdam, Netherlands.
Léa M M CostesDepartment of Pediatric Gastroenterology, Erasmus MC, University Medical Center, 3015 GE Rotterdam, Netherlands.
Junda M KelDepartment of Immunology, Erasmus MC, University Medical Center, 3015 GE Rotterdam, Netherlands.
Dicky J Lindenbergh-KortleveDepartment of Pediatric Gastroenterology, Erasmus MC, University Medical Center, 3015 GE Rotterdam, Netherlands.
Inge Brouwers-HaspelsDepartment of Immunology, Erasmus MC, University Medical Center, 3015 GE Rotterdam, Netherlands.
Astrid P HeikemaDepartment of Medical Microbiology and Infectious Diseases, Erasmus MC, University Medical Center, 3015 GE Rotterdam, Netherlands.
Janneke N SamsomDepartment of Pediatric Gastroenterology, Erasmus MC, University Medical Center, 3015 GE Rotterdam, Netherlands.
Björn E ClausenDepartment of Immunology, Erasmus MC, University Medical Center, 3015 GE Rotterdam, Netherlands.
Erasmus MC · NLUniversity Medical Center of the Johannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although IL-10 promotes a regulatory phenotype of CD11c+ dendritic cells and macrophages in vitro, the role of IL-10 signaling in CD11c+ cells to maintain intestinal tolerance in vivo remains elusive. To this aim, we generated mice with a CD11c-specific deletion of the IL-10 receptor alpha (Cd11ccreIl10rafl/fl). In contrast to the colon, the small intestine of Cd11ccreIl10rafl/fl mice exhibited spontaneous crypt hyperplasia, increased numbers of intraepithelial lymphocytes and lamina propria T cells, associated with elevated levels of T cell-derived IFNγ and IL-17A. Whereas naive mucosal T-cell priming was not affected and oral tolerance to ovalbumin was intact, augmented T-cell function in the lamina propria was associated with elevated numbers of locally dividing T cells, expression of T-cell attracting chemokines and reduced T-cell apoptosis. Upon stimulation, intestinal IL-10Rα deficient CD11c+ cells exhibited increased activation associated with enhanced IL-6 and TNFα production. Following colonization with Helicobacter hepaticus Cd11ccreIl10rafl/fl mice developed severe large intestinal inflammation characterized by infiltrating T cells and increased levels of Il17a, Ifng, and Il12p40. Altogether these findings demonstrate a critical role of IL-10 signaling in CD11c+ cells to control small intestinal immune homeostasis by limiting reactivation of local memory T cells and to protect against Helicobacter hepaticus-induced colitis.

Indexed as

Immunity, MucosalAnimalsCD11c AntigenColitisDisease Models, AnimalGenetic Predisposition to DiseaseHelicobacter hepaticusHelicobacter InfectionsHomeostasisImmunologic MemoryInterferon-gammaInterleukin-10Interleukin-10 Receptor alpha SubunitInterleukin-17Intestinal MucosaIntestine, LargeCD11c AntigenIFNG protein, mouseIL10 protein, mouseIl17a protein, mouseInterferon-gammaInterleukin-10Interleukin-10 Receptor alpha SubunitInterleukin-17CD11c+ myeloid cellsceliac diseasedendritic cellsinterleukin 10small intestine

Identifiers

PMID27027442
PMCPMC5077993
OpenAlexW2319155690

What OpenQuestion holds

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LicenceCC BY
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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.