Evidence map›Paper›PMID 24985083›Full record

ArticleMucosal immunology2015

Dedicated immunosensing of the mouse intestinal epithelium facilitated by a pair of genetically coupled lectin-like receptors.

S Leibelt, M E Friede, C Rohe, D Gütle, E Rutkowski, A Weigert, L Kveberg, J T Vaage, M W Hornef, A Steinle

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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 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 21 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 3 institutions in 2 countries.

S LeibeltInstitute for Molecular Medicine, Goethe-University Frankfurt am Main, Frankfurt am Main, Germany.
M E FriedeInstitute for Molecular Medicine, Goethe-University Frankfurt am Main, Frankfurt am Main, Germany.
C RoheInstitute for Molecular Medicine, Goethe-University Frankfurt am Main, Frankfurt am Main, Germany.
D GütleInstitute for Medical Microbiology and Hospital Epidemiology, Hannover Medical School, Hannover, Germany.
E RutkowskiInstitute for Molecular Medicine, Goethe-University Frankfurt am Main, Frankfurt am Main, Germany.
A WeigertInstitute for Biochemistry I, Goethe-University Frankfurt am Main, Frankfurt am Main, Germany.
L KvebergDepartment of Immunology, Oslo University Hospital, Rikshospitalet and University of Oslo, Oslo, Norway.
J T VaageDepartment of Immunology, Oslo University Hospital, Rikshospitalet and University of Oslo, Oslo, Norway.
M W HornefInstitute for Medical Microbiology and Hospital Epidemiology, Hannover Medical School, Hannover, Germany.
A SteinleInstitute for Molecular Medicine, Goethe-University Frankfurt am Main, Frankfurt am Main, Germany.
Goethe University Frankfurt · DEMedizinische Hochschule Hannover · DEOslo University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The integrity of the intestinal epithelium is constantly surveyed by a peculiar subset of innate-like T lymphocytes embedded in the epithelial cell layer, hence called intestinal intraepithelial lymphocytes (IELs). IELs are thought to act as "first-line" sentinels sensing the state of adjacent epithelial cells via both T-cell receptors and auxiliary receptors. Auxiliary receptors modulating IEL activity include C-type lectin-like receptors encoded in the natural killer gene complex such as NKG2D. Here, we report that the CTLR Nkrp1g is expressed by a subpopulation of mouse CD103(+) IELs allowing immunosensing of the intestinal epithelium through ligation of the genetically coupled CTLR Clr-f that is almost exclusively expressed on differentiated intestinal epithelial cells (IECs). Most of these Nkrp1g-expressing IELs exhibit a γδTCR(bright)Nkg2a(-) phenotype and are intimately associated with the intestinal epithelium. As Clr-f expression strongly inhibits effector functions of Nkrp1g-expressing cells and is upregulated upon poly(I:C) challenge, Clr-f molecules may quench reactivity of these IELs towards the epithelial barrier that is constantly provoked by microbial and antigenic stimuli. Altogether, we here newly characterize a genetically linked C-type lectin-like receptor/ligand pair with a highly restricted tissue expression that apparently evolved to allow for a dedicated immunosurveillance of the mouse intestinal epithelium.

Indexed as

AnimalsCell LineEpithelial CellsFemaleGene ExpressionHumansImmunophenotypingIntestinal MucosaLectins, C-TypeLymphocytesMiceMultigene FamilyNK Cell Lectin-Like Receptor Subfamily BOrgan SpecificityPeyer's PatchesPhenotypeLectins, C-TypeNK Cell Lectin-Like Receptor Subfamily BPoly I-CReceptors, Antigen, T-Cell

Identifiers

PMID24985083
OpenAlexW1963499915

What OpenQuestion holds

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Registered trials

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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.