Evidence map›Paper›PMID 25100292›Full record

ArticleMucosal immunology2015

Transcription factor c-Rel plays a crucial role in driving anti-CD40-mediated innate colitis.

A Visekruna, T Linnerz, V Martinic, N Vachharajani, S Hartmann, H Harb, T Joeris, P I Pfefferle, M J Hofer, U Steinhoff

Open access · bronzeAbstract read
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In one paragraph

Article in Mucosal immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

10 citing papers in PubMed, 17 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

10 authors at 4 institutions in 3 countries.

A Visekruna1] Institute for Medical Microbiology and Hygiene, Philipps University of Marburg, Marburg, Germany [2] Max Planck Institute for Infection Biology, Department of Immunology, Berlin, Germany.
T LinnerzInstitute for Medical Microbiology and Hygiene, Philipps University of Marburg, Marburg, Germany.
V MartinicInstitute for Medical Microbiology and Hygiene, Philipps University of Marburg, Marburg, Germany.
N VachharajaniInstitute for Medical Microbiology and Hygiene, Philipps University of Marburg, Marburg, Germany.
S HartmannInstitute for Medical Microbiology and Hygiene, Philipps University of Marburg, Marburg, Germany.
H HarbInstitute of Laboratory Medicine and Pathobiochemistry, Molecular Diagnostics, Philipps University of Marburg, Marburg, Germany.
T Joeris1] Max Planck Institute for Infection Biology, Department of Immunology, Berlin, Germany [2] Immunology Section, Department of Experimental Medical Science, Lund University, Lund, Sweden.
P I PfefferleMax Planck Institute for Infection Biology, Department of Immunology, Berlin, Germany.
M J Hofer1] Department of Neuropathology, Philipps University of Marburg, Marburg, Germany [2] School of Molecular Bioscience, The University of Sydney, Darlington, New South Wales, Australia.
U Steinhoff1] Institute for Medical Microbiology and Hygiene, Philipps University of Marburg, Marburg, Germany [2] Max Planck Institute for Infection Biology, Department of Immunology, Berlin, Germany.
Philipps University of Marburg · DELund University · SEMax Planck Institute for Infection Biology · DEThe University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic and environmental factors, including the commensal microbiota, have a crucial role in the development of inflammatory bowel disease. Aberrant activation of the transcription factor NF-κB is associated with chronic intestinal inflammation in mice and humans. Recently, an emerging family of innate lymphoid cells (ILCs) has been identified at mucosal sites contributing to the maintenance of gut homeostasis and intestinal immunopathology. Here, we show that the NF-κB protein c-Rel regulates the inflammatory potential of colonic IFN-γ(+)Thy1(+) ILCs to induce anti-CD40-mediated colitis in rag1(-/-) mice. Stimulation of dendritic cells (DCs) with anti-CD40 or CD40L led to translocation of c-Rel into the nucleus resulting in induction of expression of interleukin-12 (IL-12) and IL-23, key regulators of innate cell-induced colitis. While c-Rel deficiency completely abrogated anti-CD40-induced colitis, adoptively transferred wild-type DCs were able to induce pronounced colonic inflammation in rag1(-/-)rel(-/-) mice. In summary, these results suggest that the expression of c-Rel in DCs is essential for initiating anti-CD40-mediated intestinal pathogenesis.

Indexed as

Immunity, InnateAnimalsCD40 AntigensColitisCytokinesDendritic CellsDisease Models, AnimalHumansInflammation MediatorsInterferon-gammaLymphocytesMiceMice, KnockoutNF-kappa BProtein BindingProto-Oncogene Proteins c-relCD40 AntigensCytokinesInflammation MediatorsInterferon-gammaNF-kappa BProto-Oncogene Proteins c-relTranscription Factors

Identifiers

PMID25100292
OpenAlexW2044047012

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.