Evidence map›Paper›PMID 21918196›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

Th17 cytokines are critical for respiratory syncytial virus-associated airway hyperreponsiveness through regulation by complement C3a and tachykinins.

Monali M Bera, Bao Lu, Thomas R Martin, Shun Cui, Lawrence M Rhein, Craig Gerard, Norma P Gerard

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06203470 (Efficacy and Safety of Mesobotox as a Potential New Therapeutic Modality of Psoriasis Vulgaris in Comparison/Combination With Topical Calcineurin Inhibitor), which is not on this map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.0field-weighted citation impact, top 6% 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.

NCT06203470 phase4not yet recruitingnot on this mapstarted 2024, after this paper: background citation

Efficacy and Safety of Mesobotox as a Potential New Therapeutic Modality of Psoriasis Vulgaris in Comparison/Combination With Topical Calcineurin Inhibitor

TypeinterventionalSponsorAssiut UniversityRan2024 to 2026Enrolled60ConditionsPsoriasis VulgarisArmsBotulinum Toxin-A, Tacrolimus
3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 59 citations in OpenAlex.

  1. Early-life respiratory syncytial virus infection and asthma.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
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  7. Murine cytomegalovirus promotes renal allograft inflammation via Th1/17 cells and IL-17A.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2022
    Article
  8. Review
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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 4 institutions in 2 countries.

Monali M BeraIna Sue Perlmutter Laboratory, Division of Respiratory Diseases, Department of Pediatrics, Children's Hospital, Boston, MA 02115, USA.
Bao Lu
Thomas R Martin
Shun Cui
Lawrence M Rhein
Craig Gerard
Norma P Gerard
Harvard University · USBeth Israel Deaconess Medical Center · USBoston Children's Hospital · USWuhan Union Hospital · CN

Funding

ASTHMA, AIRWAY INFLAMMATION AND BETA CHEMOKINE RECEPTORSR01AI039759 · NIAID · CHILDREN'S HOSPITAL BOSTON · PI GERARD, CRAIG · 1996 to 2013
$4.1M
NIAID NIH HHS AI039759NIAID NIH HHS R01 AI039759
6 · The paper itself

Abstract

Respiratory syncytial virus (RSV) infection is associated with serious lung disease in infants and immunocompromised individuals and is linked to development of asthma. In mice, acute RSV infection causes airway hyperresponsiveness (AHR), inflammation, and mucus hypersecretion. Infected cells induce complement activation, producing the anaphylatoxin C3a. In this paper, we show RSV-infected wild-type mice produce Th17 cytokines, a response not previously associated with viral infections. Mice deficient in the C3aR fail to develop AHR following acute RSV infection, and production of Th17 cytokines was significantly attenuated. Tachykinin production also has been implicated in RSV pathophysiology, and tachykinin receptor-null mice were similarly protected from developing AHR. These animals were also deficient in production of Th17 cytokines. Tachykinin release was absent in mice deficient in C3aR, whereas C3a levels were unchanged in tachykinin receptor-null animals. Thus, our data reveal a crucial sequence following acute RSV infection where initial C3a production causes tachykinin release, followed by activation of the IL-17A pathway. Deficiency of either receptor affords protection from AHR, identifying two potential therapeutic targets.

Indexed as

AnimalsBronchial HyperreactivityCell SeparationComplement C3aCytokinesEnzyme-Linked Immunosorbent AssayFlow CytometryGene ExpressionGene Expression ProfilingInterleukin-17MiceMice, KnockoutRespiratory Syncytial VirusesRespiratory Syncytial Virus InfectionsReverse Transcriptase Polymerase Chain ReactionTachykininsComplement C3aCytokinesInterleukin-17Tachykinins

Identifiers

PMID21918196
PMCPMC3186836
OpenAlexW2161165188

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.