Evidence map›Paper›PMID 30143589›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2018

Differential Induction of IFN-α and Modulation of CD112 and CD54 Expression Govern the Magnitude of NK Cell IFN-γ Response to Influenza A Viruses.

Lisa M Kronstad, Christof Seiler, Rosemary Vergara, Susan P Holmes, Catherine A Blish

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 46 citations in OpenAlex.

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  16. A robust and interpretable end-to-end deep learning model for cytometry data.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  17. Article
  18. Dynamic Natural Killer Cell and T Cell Responses to Influenza Infection.Frontiers in cellular and infection microbiology · 2020
    Review
  19. Article
  20. Article
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

5 authors at 2 institutions in 1 country.

Lisa M KronstadDivision of Infectious Diseases and Geographic Medicine, Department of Medicine, School of Medicine, Stanford University, Stanford, CA 94305.ORCID 0000-0002-8866-3006
Christof SeilerDepartment of Statistics, Stanford University, Stanford, CA 94305.ORCID 0000-0001-8802-3642
Rosemary VergaraImmunology Program, School of Medicine, Stanford University Stanford, CA 94305; and.ORCID 0000-0001-5406-3785
Susan P HolmesDepartment of Statistics, Stanford University, Stanford, CA 94305.ORCID 0000-0002-2208-8168
Catherine A BlishDivision of Infectious Diseases and Geographic Medicine, Department of Medicine, School of Medicine, Stanford University, Stanford, CA 94305; cblish@stanford.edu.
Stanford University · USChan Zuckerberg Biohub San Francisco · US

Funding

Using a tonsil organoid system to probe conditions for the induction of protective antibody and T cell responses to influenza.U19AI057229 · NIAID · STANFORD UNIVERSITY · PI Mark Morris Davis · 2003 to 2026
$88.5M
MOLECULAR &CELLULAR IMMUNOBIOLOGYT32AI007290 · NIAID · STANFORD UNIVERSITY · PI Sean Curtis Bendall, Olivia M Martinez · 1985 to 2026
$27.0M
Modeling the influence of sex on natural killer cell networksDP2AI112193 · NIAID · STANFORD UNIVERSITY · PI BLISH, CATHERINE A · 2013 to 2015
$2.5M
Impact of HIV exposure, feeding status, and microbiome on immune ontogeny and vaccine responses in infantsU01AI131302 · NIAID · STANFORD UNIVERSITY · PI BLISH, CATHERINE A, GRAY, CLIVE MAURICE · 2017 to 2021
$2.1M
Shaping Natural Killer repertoires and HIV responsiveness via antigen exposureR56AI124788 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI BLISH, CATHERINE A, PAUST, SILKE · 2016 to 2016
$738k
CyTOF Mass CytometerS10RR027582 · NCRR · STANFORD UNIVERSITY · PI NOLAN, GARRY P · 2010 to 2010
$500k
Diagnostic signatures of Zika virus pathogenesisR21AI130523 · NIAID · STANFORD UNIVERSITY · PI BLISH, CATHERINE A · 2017 to 2018
$400k
NCRR NIH HHS S10 RR027582NIAID NIH HHS DP2 AI112193NIAID NIH HHS R21 AI130523NIAID NIH HHS R56 AI124788NIAID NIH HHS T32 AI007290NIAID NIH HHS U01 AI131302NIAID NIH HHS U19 AI057229
6 · The paper itself

Abstract

In human and murine studies, IFN-γ is a critical mediator immunity to influenza. IFN-γ production is critical for viral clearance and the development of adaptive immune responses, yet excessive production of IFN-γ and other cytokines as part of a cytokine storm is associated with poor outcomes of influenza infection in humans. As NK cells are the main population of lung innate immune cells capable of producing IFN-γ early in infection, we set out to identify the drivers of the human NK cell IFN-γ response to influenza A viruses. We found that influenza triggers NK cells to secrete IFN-γ in the absence of T cells and in a manner dependent upon signaling from both cytokines and receptor-ligand interactions. Further, we discovered that the pandemic A/California/07/2009 (H1N1) strain elicits a seven-fold greater IFN-γ response than other strains tested, including a seasonal A/Victoria/361/2011 (H3N2) strain. These differential responses were independent of memory NK cells. Instead, we discovered that the A/Victoria/361/2011 influenza strain suppresses the NK cell IFN-γ response by downregulating NK-activating ligands CD112 and CD54 and by repressing the type I IFN response in a viral replication-dependent manner. In contrast, the A/California/07/2009 strain fails to repress the type I IFN response or to downregulate CD54 and CD112 to the same extent, which leads to the enhanced NK cell IFN-γ response. Our results indicate that influenza implements a strain-specific mechanism governing NK cell production of IFN-γ and identifies a previously unrecognized influenza innate immune evasion strategy.

Indexed as

AnimalsCells, CulturedGene Expression RegulationHumansImmune EvasionImmunity, InnateInfluenza A Virus, H1N1 SubtypeInfluenza A Virus, H3N2 SubtypeInfluenza, HumanIntercellular Adhesion Molecule-1Interferon-alphaInterferon-gammaKiller Cells, NaturalLungMiceNectinsIntercellular Adhesion Molecule-1Interferon-alphaInterferon-gammaNectins

Identifiers

PMID30143589
PMCPMC6143432
OpenAlexW2888038294

What OpenQuestion holds

Textmetadata
LicenceTDM
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.