Evidence map›Paper›PMID 29497422›Full record

ArticleFrontiers in immunology2018

Respiratory Influenza A Virus Infection Triggers Local and Systemic Natural Killer Cell Activation

Sabine Stegemann-Koniszewski, Sarah Behrens, Julia D Boehme, Inga Hochnadel, Peggy Riese, Carlos A Guzmán, Andrea Kröger, Jens Schreiber, Matthias Gunzer, Dunja Bruder

Abstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
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

28 citing papers in PubMed.

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  16. Triphasic production of IFNDiscovery immunology · 2023
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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.

Sabine Stegemann-KoniszewskiImmune Regulation, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Sarah BehrensImmune Regulation, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Julia D BoehmeImmune Regulation, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Inga HochnadelImmune Regulation, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Peggy RieseDepartment of Vaccinology and Applied Microbiology, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Carlos A GuzmánDepartment of Vaccinology and Applied Microbiology, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Andrea KrögerMolecular Microbiology, Institute of Medical Microbiology, Infection Control and Prevention, Health Campus Immunology, Infectiology and Inflammation, Otto-von-Guericke University, Magdeburg, Germany.
Jens SchreiberExperimental Pneumology, University Hospital of Pneumology, University Hospital Magdeburg, Health Campus Immunology, Infectiology and Inflammation, Otto-von-Guericke University, Magdeburg, Germany.
Matthias GunzerInstitute for Experimental Immunology and Imaging, University Hospital, University of Duisburg-Essen, Essen, Germany.
Dunja BruderImmune Regulation, Helmholtz Centre for Infection Research, Braunschweig, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The innate immune system senses influenza A virus (IAV) through different pathogen-recognition receptors including Toll-like receptor 7 (TLR7). Downstream of viral recognition natural killer (NK) cells are activated as part of the anti-IAV immune response. Despite the known decisive role of TLR7 for NK cell activation by therapeutic immunostimulatory RNAs, the contribution of TLR7 to the NK cell response following IAV infection has not been addressed. We have analyzed lung cytokine responses as well as the activation, interferon (IFN)-γ production, and cytotoxicity of lung and splenic NK cells following sublethal respiratory IAV infection in wild-type and TLR7ko mice. Early airway IFN-γ levels as well as the induction of lung NK cell CD69 expression and IFN-γ production in response to IAV infection were significantly attenuated in TLR7-deficient hosts. Strikingly, respiratory IAV infection also primed splenic NK cells for IFN-γ production, degranulation, and target cell lysis, all of which were fully dependent on TLR7. At the same time, lung type I IFN levels were significantly reduced in TLR7ko mice early following IAV infection, displaying a potential upstream mechanism of the attenuated NK cell activation observed. Taken together, our data clearly demonstrate a specific role for TLR7 signaling in local and systemic NK cell activation following respiratory IAV infection despite the presence of redundant innate IAV-recognition pathways.

Indexed as

AnimalsCell DegranulationDisease Models, AnimalDogsFemaleHumansImmunity, InnateInfluenza A virusInfluenza, HumanInterferon-gammaKiller Cells, NaturalLungLymphocyte ActivationMadin Darby Canine Kidney CellsMembrane GlycoproteinsMiceIFNG protein, mouseInterferon-gammaMembrane GlycoproteinsTlr7 protein, mouseToll-Like Receptor 7influenza A virusinnate immunitynatural killer cellspathogen-recognition receptorsrespiratory infectionToll-like receptor 7

Identifiers

PMID29497422
PMCPMC5819576

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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.