Evidence map›Paper›PMID 21703407›Full record

ArticleThe American journal of pathology2011

IL-17-induced pulmonary pathogenesis during respiratory viral infection and exacerbation of allergic disease.

Sumanta Mukherjee, Dennis M Lindell, Aaron A Berlin, Susan B Morris, Thomas P Shanley, Marc B Hershenson, Nicholas W Lukacs

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 152 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
152citing papers in PubMed, 2 pooled it
12.6field-weighted citation impact, top 1% 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

152 citing papers in PubMed, 2 syntheses or guidelines pooled it, 239 citations in OpenAlex.

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  5. Early-life respiratory syncytial virus infection and asthma.European respiratory review : an official journal of the European Respiratory Society · 2026
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  7. Hypoxia inducible factors regulate pneumovirus replication by enhancing innate immune sensing.Proceedings of the National Academy of Sciences of the United States of America · 2026
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92 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

7 authors at 1 institution in 1 country.

Sumanta MukherjeeDepartment of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Dennis M Lindell
Aaron A Berlin
Susan B Morris
Thomas P Shanley
Marc B Hershenson
Nicholas W Lukacs
University of Michigan · US

Funding

The Role of C-C Chemokines in Eosinophil Airway InflammationR01AI036302 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUKACS, NICHOLAS W · 2001 to 2018
$5.6M
TLR and Notch Ligand in RSV-induced DiseaseR01AI073876 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUKACS, NICHOLAS W · 2008 to 2012
$1.9M
C-C CHEMOKINES AND EOSINOPHIL AIRWAY INFLAMMATIONR29AI036302 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUKACS, NICHOLAS W · 1996 to 2000
$107k
NIAID NIH HHS AI-036302NIAID NIH HHS AI-073876NIAID NIH HHS R01 AI036302NIAID NIH HHS R01 AI073876NIAID NIH HHS R29 AI036302
6 · The paper itself

Abstract

Severe respiratory syncytial virus (RSV) infections are characterized by airway epithelial cell damage, mucus hypersecretion, and Th2 cytokine production. Less is known about the role of IL-17. We observed increased IL-6 and IL-17 levels in tracheal aspirate samples from severely ill infants with RSV infection. In a mouse model of RSV infection, time-dependent increases in pulmonary IL-6, IL-23, and IL-17 expression were observed. Neutralization of IL-17 during infection and observations from IL-17(-/-) knockout mice resulted in significant inhibition of mucus production during RSV infection. RSV-infected animals treated with anti-IL-17 had reduced inflammation and decreased viral load, compared with control antibody-treated mice. Blocking IL-17 during infection resulted in significantly increased RSV-specific CD8 T cells. Factors associated with CD8 cytotoxic T lymphocytes, T-bet, IFN-γ, eomesodermin, and granzyme B were significantly up-regulated after IL-17 blockade. Additionally, in vitro analyses suggest that IL-17 directly inhibits T-bet, eomesodermin, and IFN-γ in CD8 T cells. The role of IL-17 was also investigated in RSV-induced exacerbation of allergic airway responses, in which neutralization of IL-17 led to a significant decrease in the exacerbated disease, including reduced mucus production and Th2 cytokines, with decreased viral proteins. Taken together, our data demonstrate that IL-17 plays a pathogenic role during RSV infections.

Indexed as

Disease Models, AnimalAnimalsAntibodies, MonoclonalBlotting, WesternCD8-Positive T-LymphocytesFemaleFlow CytometryGranzymesHumansHypersensitivityInflammationInterferon-gammaInterleukin-17Interleukin-23Lung DiseasesMiceAntibodies, MonoclonalGranzymesInterferon-gammaInterleukin-17Interleukin-23RNA, MessengerViral Proteins

Identifiers

PMID21703407
PMCPMC3123803
OpenAlexW1968715103

What OpenQuestion holds

Textmetadata
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.