Evidence map›Paper›PMID 29898768›Full record

ArticleGenome medicine2018

KLRD1-expressing natural killer cells predict influenza susceptibility.

Erika Bongen, Francesco Vallania, Paul J Utz, Purvesh Khatri

Open access · goldAbstract read
In one paragraph

Article in Genome medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

52 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
  2. Article
  3. Multivariate Host-Pathogen Interactions Driving Heterogeneous Viral Shedding and CD8medRxiv : the preprint server for health sciences · 2025
    Article
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  15. Gene Expression in Cord Blood and Tuberculosis in Early Childhood: A Nested Case-Control Study in a South African Birth Cohort.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2023
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Upregulated CD8Frontiers in immunology · 2023
    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

4 authors at 2 institutions in 1 country.

Erika BongenInstitute for Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA, 94305, USA.ORCID 0000-0001-8429-7742
Francesco VallaniaInstitute for Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA, 94305, USA.
Paul J UtzInstitute for Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA, 94305, USA.
Purvesh KhatriInstitute for Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA, 94305, USA. pkhatri@stanford.edu.
Stanford Medicine · USStanford University · 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
Translational Incubator CoreU19AI109662 · NIAID · STANFORD UNIVERSITY · PI GLENN, JEFFREY S · 2014 to 2019
$28.6M
MOLECULAR &CELLULAR IMMUNOBIOLOGYT32AI007290 · NIAID · STANFORD UNIVERSITY · PI Sean Curtis Bendall, Olivia M Martinez · 1985 to 2026
$27.0M
Vaccination and infection: indicators of immunological health and responsivenessU19AI090019 · NIAID · STANFORD UNIVERSITY · PI DAVIS, MARK MORRIS · 2010 to 2015
$17.3M
Giant MagnetoResistive (GMR) Sensors for Measuring Influenza VaccineR01AI125197 · NIAID · STANFORD UNIVERSITY · PI UTZ, PAUL JOSEPH, WANG, SHAN X. · 2016 to 2021
$5.0M
Ultra-Fast Epigenomic Maps for Monitoring AutoimmunityU19AI110491 · NIAID · STANFORD UNIVERSITY · PI MAECKER, HOLDEN T. · 2014 to 2018
$3.6M
Stanford Career Development Program in Omics of Lung DiseasesK12HL120001 · NHLBI · STANFORD UNIVERSITY · PI NICOLLS, MARK ROBERT, RABINOVITCH, MARLENE · 2013 to 2017
$1.3M
National Institute of Allergy and Infectious Diseases 1U19AI109662National Institute of Allergy and Infectious Diseases 1U19AI110491-01National Institute of Allergy and Infectious Diseases U19AI057229NHLBI NIH HHS K12 HL120001NIAID NIH HHS R01 AI125197NIAID NIH HHS U19 AI057229NIAID NIH HHS U19 AI090019NIAID NIH HHS U19 AI109662NIAID NIH HHS U19 AI110491NIH HHS 5K12HL120001-02NIH HHS R01 AI125197-01NIH HHS U19AI090019
6 · The paper itself

Abstract

backgroundInfluenza infects tens of millions of people every year in the USA. Other than notable risk groups, such as children and the elderly, it is difficult to predict what subpopulations are at higher risk of infection. Viral challenge studies, where healthy human volunteers are inoculated with live influenza virus, provide a unique opportunity to study infection susceptibility. Biomarkers predicting influenza susceptibility would be useful for identifying risk groups and designing vaccines.

methodsWe applied cell mixture deconvolution to estimate immune cell proportions from whole blood transcriptome data in four independent influenza challenge studies. We compared immune cell proportions in the blood between symptomatic shedders and asymptomatic nonshedders across three discovery cohorts prior to influenza inoculation and tested results in a held-out validation challenge cohort.

resultsNatural killer (NK) cells were significantly lower in symptomatic shedders at baseline in both discovery and validation cohorts. Hematopoietic stem and progenitor cells (HSPCs) were higher in symptomatic shedders at baseline in discovery cohorts. Although the HSPCs were higher in symptomatic shedders in the validation cohort, the increase was statistically nonsignificant. We observed that a gene associated with NK cells, KLRD1, which encodes CD94, was expressed at lower levels in symptomatic shedders at baseline in discovery and validation cohorts. KLRD1 expression in the blood at baseline negatively correlated with influenza infection symptom severity. KLRD1 expression 8 h post-infection in the nasal epithelium from a rhinovirus challenge study also negatively correlated with symptom severity.

conclusionsWe identified KLRD1-expressing NK cells as a potential biomarker for influenza susceptibility. Expression of KLRD1 was inversely correlated with symptom severity. Our results support a model where an early response by KLRD1-expressing NK cells may control influenza infection.

Indexed as

Genetic Predisposition to DiseaseCohort StudiesCytoplasmic GranulesCytotoxicity, ImmunologicDatabases as TopicDendritic CellsHematopoietic Stem CellsHumansInfluenza, HumanKiller Cells, NaturalMacrophagesNasal MucosaNK Cell Lectin-Like Receptor Subfamily CNK Cell Lectin-Like Receptor Subfamily DRhinovirusKLRC3 protein, humanKLRD1 protein, humanNK Cell Lectin-Like Receptor Subfamily CNK Cell Lectin-Like Receptor Subfamily DCD94Hematopoietic stem and progenitor cellsInfluenzaKLRD1Natural killer cells

Identifiers

PMID29898768
PMCPMC6001128
OpenAlexW2805822392

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.