Evidence map›Paper›PMID 24068930›Full record

ArticlePLoS pathogens2013

Group 2 innate lymphoid cell production of IL-5 is regulated by NKT cells during influenza virus infection.

Stacey Ann Gorski, Young S Hahn, Thomas J Braciale

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 1 pooled it
6.5field-weighted citation impact, top 3% 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

101 citing papers in PubMed, 1 synthesis or guideline pooled it, 152 citations in OpenAlex.

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41 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Stacey Ann GorskiBeirne B. Carter Center for Immunology Research, University of Virginia, Charlottesville, Virginia, United States of America ; Department of Microbiology, University of Virginia, Charlottesville, Virginia, United States of America.
Young S Hahn
Thomas J Braciale
Carter Center · USUniversity of Virginia · US

Funding

INTERDISCIPLINARY TRAINING PROGRAM IN IMMUNOLOGYT32AI007496 · NIAID · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Michael G. Brown, Coleen A McNamara · 1995 to 2026
$10.2M
Regulation of CD8+ T cell responses via liver NK-DC crosstalkU19AI083024 · NIAID · UNIVERSITY OF VIRGINIA · PI LANNIGAN, JOANNE A · 2009 to 2013
$8.1M
BIOTECHNOLOGY TRAINING PROGRAMT32GM008715 · NIGMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI LAURIE, GORDON WILLIAM · 2000 to 2019
$6.6M
CYTOTOXIC T LYMPHOCYTE RESPONSE TO INFLUENZA VIRUSR01AI015608 · NIAID · WASHINGTON UNIVERSITY · PI BRACIALE, THOMAS J · 1985 to 2017
$5.7M
T Cell Function in Pulmonary Viral Pulmonary Infection and InjuryR01HL033391 · NHLBI · WASHINGTON UNIVERSITY · PI BRACIALE, THOMAS J · 1985 to 2012
$4.3M
IMMUNOBIOLOGY OF EXPERIMENTAL RSV INFECTIONR01AI037293 · NIAID · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI BRACIALE, THOMAS J · 1994 to 2007
$2.3M
NHLBI NIH HHS R01 HL033391NHLBI NIH HHS R01 HL-33391NIAID NIH HHS R01 AI015608NIAID NIH HHS R01 AI037293NIAID NIH HHS R01 AI-15608NIAID NIH HHS R01 AI-37293NIAID NIH HHS T32 AI007496NIAID NIH HHS T32 AI-07496NIAID NIH HHS U-10 AI-83024NIAID NIH HHS U19 AI083024NIGMS NIH HHS T32 GM008715NIGMS NIH HHS T32 GM-8715
6 · The paper itself

Abstract

Respiratory virus infections, such as influenza, typically induce a robust type I (pro-inflammatory cytokine) immune response, however, the production of type 2 cytokines has been observed. Type 2 cytokine production during respiratory virus infection is linked to asthma exacerbation; however, type 2 cytokines may also be tissue protective. Interleukin (IL)-5 is a prototypical type 2 cytokine that is essential for eosinophil maturation and egress out of the bone marrow. However, little is known about the cellular source and underlying cellular and molecular basis for the regulation of IL-5 production during respiratory virus infection. Using a mouse model of influenza virus infection, we found a robust transient release of IL-5 into infected airways along with a significant and progressive accumulation of eosinophils into the lungs, particularly during the recovery phase of infection, i.e. following virus clearance. The cellular source of the IL-5 was group 2 innate lymphoid cells (ILC2) infiltrating the infected lungs. Interestingly, the progressive accumulation of eosinophils following virus clearance is reflected in the rapid expansion of c-kit⁺ IL-5 producing ILC2. We further demonstrate that the enhanced capacity for IL-5 production by ILC2 during recovery is concomitant with the enhanced expression of the IL-33 receptor subunit, ST2, by ILC2. Lastly, we show that NKT cells, as well as alveolar macrophages (AM), are endogenous sources of IL-33 that enhance IL-5 production from ILC2. Collectively, these results reveal that c-kit⁺ ILC2 interaction with IL-33 producing NKT and AM leads to abundant production of IL-5 by ILC2 and accounts for the accumulation of eosinophils observed during the recovery phase of influenza infection.

Indexed as

AnimalsCells, CulturedEosinophiliaEosinophilsImmunity, InnateInfluenza A Virus, H1N1 SubtypeInterleukin-33Interleukin-5InterleukinsKiller Cells, NaturalLungMacrophages, AlveolarMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutOrthomyxoviridae InfectionsIl33 protein, mouseInterleukin-33Interleukin-5InterleukinsProtein SubunitsReceptors, Interleukin

Identifiers

PMID24068930
PMCPMC3777868
OpenAlexW2011987715

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.