Evidence map›Paper›PMID 28051086›Full record

ArticleMucosal immunology2017

Neutrophilic NLRP3 inflammasome-dependent IL-1β secretion regulates the γδT17 cell response in respiratory bacterial infections.

M Hassane, D Demon, D Soulard, J Fontaine, L E Keller, E C Patin, R Porte, I Prinz, B Ryffel, A Kadioglu and 6 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Mucosal immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

37 citing papers in PubMed, 58 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

16 authors at 5 institutions in 6 countries.

M HassaneUniv. Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, U1019-UMR 8204-CIIL-Center for Infection and Immunity of Lille, Lille, France.
D DemonInflammation Research Center, VIB, Zwijnaarde, Belgium.
D SoulardUniv. Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, U1019-UMR 8204-CIIL-Center for Infection and Immunity of Lille, Lille, France.
J FontaineUniv. Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, U1019-UMR 8204-CIIL-Center for Infection and Immunity of Lille, Lille, France.
L E KellerMolecular Genetics Group, Groningen Biomolecular Sciences and Biotechnology Institute, Centre for Synthetic Biology, University of Groningen, Groningen, The Netherlands.
E C PatinUniv. Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, U1019-UMR 8204-CIIL-Center for Infection and Immunity of Lille, Lille, France.
R PorteUniv. Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, U1019-UMR 8204-CIIL-Center for Infection and Immunity of Lille, Lille, France.
I PrinzInstitute of Immunology, Hannover Medical School, Hannover, Germany.
B RyffelCNRS, UMR7355, Experimental and Molecular Immunology and Neurogenetics, University, Orléans, France and IDM, University of Cape Town, RSA.
A KadiogluDepartment of Clinical Infection, Institute of Infection and Global Health, University of Liverpool, Liverpool, UK.
J-W VeeningMolecular Genetics Group, Groningen Biomolecular Sciences and Biotechnology Institute, Centre for Synthetic Biology, University of Groningen, Groningen, The Netherlands.
J-C SirardUniv. Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, U1019-UMR 8204-CIIL-Center for Infection and Immunity of Lille, Lille, France.
C FaveeuwUniv. Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, U1019-UMR 8204-CIIL-Center for Infection and Immunity of Lille, Lille, France.
M LamkanfiInflammation Research Center, VIB, Zwijnaarde, Belgium.
F TrotteinUniv. Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, U1019-UMR 8204-CIIL-Center for Infection and Immunity of Lille, Lille, France.
C PagetUniv. Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, U1019-UMR 8204-CIIL-Center for Infection and Immunity of Lille, Lille, France.
Centre National de la Recherche Scientifique · FRGhent University · BEUniversity of Groningen · NLMedizinische Hochschule Hannover · DEUniversity of Liverpool · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traditionally regarded as simple foot soldiers of the innate immune response limited to the eradication of pathogens, neutrophils recently emerged as more complex cells endowed with a set of immunoregulatory functions. Using a model of invasive pneumococcal disease, we highlighted an unexpected key role for neutrophils as accessory cells in innate interleukin (IL)-17A production by lung resident Vγ6Vδ1

Indexed as

AnimalsBacterial ProteinsCells, CulturedDisease Models, AnimalHumansInflammasomesInterleukin-17Interleukin-1betaMacrophages, AlveolarMaleMiceMice, Inbred C57BLMice, KnockoutNeutrophilsNLR Family, Pyrin Domain-Containing 3 ProteinPneumococcal InfectionsBacterial ProteinsInflammasomesInterleukin-17Interleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinplY protein, Streptococcus pneumoniaeReceptors, Antigen, T-Cell, gamma-deltaStreptolysinsTumor Necrosis Factor-alpha

Identifiers

PMID28051086
OpenAlexW2571029248

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.