Evidence map›Paper›PMID 30427069›Full record

ArticleEuropean journal of immunology2019

Innate and adaptive stimulation of murine diverse NKT cells result in distinct cellular responses.

Prabhanshu Tripathi, Saikiran K Sedimbi, Avadhesh Kumar Singh, Linda Löfbom, Shohreh Issazadeh-Navikas, Siegfried Weiss, Irmgard Förster, Mikael C I Karlsson, Ulf Yrlid, Nadir Kadri and 1 more

Open access · hybridAbstract read
In one paragraph

Article in European journal of immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.3field-weighted citation impact, top 43% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
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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

11 authors at 5 institutions in 4 countries.

Prabhanshu TripathiDepartment of Microbiology and Immunology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.
Saikiran K SedimbiDepartment of Microbiology and Immunology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.
Avadhesh Kumar SinghDepartment of Microbiology and Immunology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.
Linda LöfbomDepartment of Microbiology and Immunology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.
Shohreh Issazadeh-NavikasNeuroinflammation Unit, Biotech Research and Innovation Centre (BRIC), Faculty of Health and Medical Sciences, Copenhagen Biocentre, University of Copenhagen, Copenhagen, Denmark.
Siegfried WeissInstitute of Immunology, Medical School Hannover, Hannover, Germany.
Irmgard FörsterImmunology and Environment, Life & Medical Sciences (LIMES) Institute, University of Bonn, Bonn, Germany.
Mikael C I KarlssonDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Ulf YrlidDepartment of Microbiology and Immunology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.
Nadir KadriCenter of Hematology and Regenerative Medicine, Department of Medicine, Karolinska Institute, Stockholm, Sweden.
Susanna L CardellDepartment of Microbiology and Immunology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.ORCID 0000-0002-7665-6781
Institute for Biomedicine · ITKarolinska Institutet · SEMedizinische Hochschule Hannover · DEUniversity of Bonn · DEUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Natural killer T (NKT) cells recognize glycolipids presented on CD1d. They share features of adaptive T lymphocytes and innate NK cells, and mediate immunoregulatory functions via rapid production of cytokines. Invariant (iNKT) and diverse (dNKT) NKT cell subsets are defined by their TCR. The immunological role of dNKT cells, that do not express the invariant TCRα-chain used by iNKT cells, is less well explored than that of iNKT cells. Here, we investigated signals driving Toll-like receptor (TLR) ligand activation of TCR-transgenic murine dNKT cells. IFN-γ production by dNKT cells required dendritic cells (DC), cell-to-cell contact and presence of TLR ligands. TLR-stimulated DC activated dNKT cells to secrete IFN-γ in a CD1d-, CD80/86- and type I IFN-independent manner. In contrast, a requirement for IL-12p40, and a TLR ligand-selective dependence on IL-18 or IL-15 was observed. TLR ligand/DC stimulation provoked early secretion of pro-inflammatory cytokines by both CD62L

Indexed as

Adaptive ImmunityAnimalsAntigens, CD1dCell ProliferationCells, CulturedCytokinesImmunity, CellularImmunity, InnateLigandsLymphocytesMice, Inbred C57BLMice, KnockoutMice, TransgenicNatural Killer T-CellsToll-Like ReceptorsAntigens, CD1dCD1d antigen, mouseCytokinesLigandsToll-Like ReceptorsCD1 moleculesCytokinesDendritic cellsNKT cellsToll like receptors

Identifiers

PMID30427069
PMCPMC6587840
OpenAlexW2901721386

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.