Evidence map›Paper›PMID 24472849›Full record

ArticleMucosal immunology2014

IL-15 complexes induce NK- and T-cell responses independent of type I IFN signaling during rhinovirus infection.

A Jayaraman, D J Jackson, S D Message, R M Pearson, J Aniscenko, G Caramori, P Mallia, A Papi, B Shamji, M Edwards and 5 more

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01159782 (Human Model of Rhinovirus Induced Acute Asthma Exacerbations), which is not on this map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.7field-weighted citation impact, top 16% 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.

NCT01159782 nacompletednot on this map

Human Model of Rhinovirus Induced Acute Asthma Exacerbations

TypeinterventionalSponsorImperial College LondonRan2011 to 2014Enrolled46ConditionsRhinovirus Infection in AsthmaArmsRhinovirus infection
3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 52 citations in OpenAlex.

  1. Rhinovirus-induced CCL17 and CCL22 in Asthma Exacerbations and Differential Regulation by STAT6.American journal of respiratory cell and molecular biology · 2021
    Trial
  2. A comprehensive overview of monkeypox virus disease.Tropical medicine and health · 2026
    Review
  3. Article
  4. Monkeypox Virus and Pregnancy.Journal of medical virology · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Natural killer cells in the lung: potential role in asthma and virus-induced exacerbation?European respiratory review : an official journal of the European Respiratory Society · 2023
    Review
  10. Review
  11. Article
  12. Article
  13. Cluster analysis of nasal cytokines during rhinovirus infection identifies different immunophenotypes in both children and adults with allergic asthma.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2022
    Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Rhinovirus and Innate Immune Function of Airway Epithelium.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

15 authors at 5 institutions in 2 countries.

A Jayaraman1] Airway Disease Infection Section, National Heart and Lung Institute, Imperial College London, London, UK [2] MRC and Asthma UK Centre in Allergic Mechanisms of Asthma, London, UK [3] Centre for Respiratory Infections, Imperial College London, London, UK.
D J Jackson1] Airway Disease Infection Section, National Heart and Lung Institute, Imperial College London, London, UK [2] MRC and Asthma UK Centre in Allergic Mechanisms of Asthma, London, UK [3] Centre for Respiratory Infections, Imperial College London, London, UK [4] Imperial College Healthcare National Health Service Trust, London, UK.
S D MessageAirway Disease Infection Section, National Heart and Lung Institute, Imperial College London, London, UK.
R M Pearson1] Airway Disease Infection Section, National Heart and Lung Institute, Imperial College London, London, UK [2] MRC and Asthma UK Centre in Allergic Mechanisms of Asthma, London, UK [3] Centre for Respiratory Infections, Imperial College London, London, UK.
J Aniscenko1] Airway Disease Infection Section, National Heart and Lung Institute, Imperial College London, London, UK [2] MRC and Asthma UK Centre in Allergic Mechanisms of Asthma, London, UK [3] Centre for Respiratory Infections, Imperial College London, London, UK.
G CaramoriSezione di Malattie dell'Apparato Respiratorio, Centro per lo Studio delle Malattie Infiammatorie Croniche delle Vie Aeree e Patologie Fumo Correlate dell'Apparato Respiratorio (CEMICEF), University of Ferrara, Ferrara, Italy.
P Mallia1] Airway Disease Infection Section, National Heart and Lung Institute, Imperial College London, London, UK [2] MRC and Asthma UK Centre in Allergic Mechanisms of Asthma, London, UK [3] Centre for Respiratory Infections, Imperial College London, London, UK [4] Imperial College Healthcare National Health Service Trust, London, UK.
A PapiSezione di Malattie dell'Apparato Respiratorio, Centro per lo Studio delle Malattie Infiammatorie Croniche delle Vie Aeree e Patologie Fumo Correlate dell'Apparato Respiratorio (CEMICEF), University of Ferrara, Ferrara, Italy.
B ShamjiNovartis Institute for Biomedical Research, Horsham, UK.
M EdwardsNovartis Institute for Biomedical Research, Horsham, UK.
J WestwickNovartis Institute for Biomedical Research, Horsham, UK.
T Hansel1] Airway Disease Infection Section, National Heart and Lung Institute, Imperial College London, London, UK [2] MRC and Asthma UK Centre in Allergic Mechanisms of Asthma, London, UK [3] Centre for Respiratory Infections, Imperial College London, London, UK [4] Imperial College Healthcare National Health Service Trust, London, UK.
L A Stanciu1] Airway Disease Infection Section, National Heart and Lung Institute, Imperial College London, London, UK [2] MRC and Asthma UK Centre in Allergic Mechanisms of Asthma, London, UK [3] Centre for Respiratory Infections, Imperial College London, London, UK.
S L Johnston1] Airway Disease Infection Section, National Heart and Lung Institute, Imperial College London, London, UK [2] MRC and Asthma UK Centre in Allergic Mechanisms of Asthma, London, UK [3] Centre for Respiratory Infections, Imperial College London, London, UK [4] Imperial College Healthcare National Health Service Trust, London, UK.
N W Bartlett1] Airway Disease Infection Section, National Heart and Lung Institute, Imperial College London, London, UK [2] MRC and Asthma UK Centre in Allergic Mechanisms of Asthma, London, UK [3] Centre for Respiratory Infections, Imperial College London, London, UK.
Asthma UK · GBNational Health Service · GBNovartis (United Kingdom) · GBUniversity of Ferrara · ITGloucestershire Royal Hospital · GB

Funding

Medical Research Council G1000758Medical Research Council G1100168Wellcome Trust
6 · The paper itself

Abstract

Rhinoviruses are among the most common viruses to infect man, causing a range of serious respiratory diseases including exacerbations of asthma and COPD. Type I IFN and IL-15 are thought to be required for antiviral immunity; however, their function during rhinovirus infection in vivo is undefined. In RV-infected human volunteers, IL-15 protein expression in fluid from the nasal mucosa and in bronchial biopsies was increased. In mice, RV induced type I IFN-dependent expressions of IL-15 and IL-15Rα, which in turn were required for NK- and CD8(+) T-cell responses. Treatment with IL-15-IL-15Rα complexes (IL-15c) boosted RV-induced expression of IL-15, IL-15Rα, IFN-γ, CXCL9, and CXCL10 followed by recruitment of activated, IFN-γ-expressing NK, CD8(+), and CD4(+) T cells. Treating infected IFNAR1(-/-) mice with IL-15c similarly increased IL-15, IL-15Rα, IFN-γ, and CXCL9 (but not CXCL10) expression also followed by NK-, CD8(+)-, and CD4(+)-T-cell recruitment and activation. We have demonstrated that type I IFN-induced IFN-γ and cellular immunity to RV was mediated by IL-15 and IL-15Rα. Importantly, we also show that IL-15 could be induced via a type I IFN-independent mechanism by IL-15 complex treatment, which in turn was sufficient to drive IFN-γ expression and lymphocyte responses.

Indexed as

AnimalsDisease Models, AnimalHumansInterferon Type IInterleukin-15Killer Cells, NaturalMicePicornaviridae InfectionsRhinovirusSignal TransductionT-LymphocytesUp-RegulationInterferon Type IInterleukin-15

Identifiers

PMID24472849
PMCPMC4284198
OpenAlexW2072963589

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.