Evidence map›Paper›PMID 26688048›Full record

ArticleScientific reports2015

T cell responses are elicited against Respiratory Syncytial Virus in the absence of signalling through TLRs, RLRs and IL-1R/IL-18R.

Michelle Goritzka, Catherine Pereira, Spyridon Makris, Lydia R Durant, Cecilia Johansson

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Type I interferons induced upon respiratory viral infection impair lung metastatic initiation.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  16. MAVS Is Essential for Primary CD4Journal of virology · 2017
    Article
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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

5 authors at 1 institution in 1 country.

Michelle GoritzkaCentre for Respiratory Infections, Respiratory Infections Section, St Mary's campus, National Heart and Lung Institute, Faculty of Medicine, Imperial College London, London, W2 1PG, UK.
Catherine PereiraCentre for Respiratory Infections, Respiratory Infections Section, St Mary's campus, National Heart and Lung Institute, Faculty of Medicine, Imperial College London, London, W2 1PG, UK.
Spyridon MakrisCentre for Respiratory Infections, Respiratory Infections Section, St Mary's campus, National Heart and Lung Institute, Faculty of Medicine, Imperial College London, London, W2 1PG, UK.
Lydia R DurantCentre for Respiratory Infections, Respiratory Infections Section, St Mary's campus, National Heart and Lung Institute, Faculty of Medicine, Imperial College London, London, W2 1PG, UK.
Cecilia JohanssonCentre for Respiratory Infections, Respiratory Infections Section, St Mary's campus, National Heart and Lung Institute, Faculty of Medicine, Imperial College London, London, W2 1PG, UK.
Imperial College London · GB

Funding

Medical Research Council G0800311
6 · The paper itself

Abstract

Pattern recognition receptors (PRRs) and cytokine receptors are key players in the initiation of immune responses to infection. PRRs detecting viral RNA, such as toll like receptor (TLR)-3, -7/8, and RIG-I like receptors (RLRs; RIG-I and MDA-5), as well as cytokine receptors such as interleukin 1 receptor (IL-1R), have been implicated in responses to RNA viruses that infect the airways. The latter includes respiratory syncytial virus (RSV), a human pathogen that can cause severe lower respiratory tract infections, especially in infants. To evaluate the collective contribution of PRRs and IL-1R signalling to RSV immunity, we generated Myd88/Trif/Mavs(-/-) mice that are deficient in signalling by all TLRs, RLRs and IL-1R, as well as other cytokine receptors such as IL-18 receptor. Early production of pro-inflammatory mediators and lung infiltration by immune cells were completely abrogated in infected Myd88/Trif/Mavs(-/-) mice. However, RSV-specific CD8(+) T cells were elicited and recruited into the lungs and airways. Consistent with these findings, Myd88/Trif/Mavs(-/-) mice survived RSV infection but displayed higher viral load and weight loss. These data highlight an unappreciated level of redundancy in pathways that couple innate virus sensing to adaptive immunity, providing the host with remarkable resilience to infection.

Indexed as

Adaptor Proteins, Signal TransducingAdaptor Proteins, Vesicular TransportAnimalsHumansInfectionsMiceMice, TransgenicMyeloid Differentiation Factor 88Receptors, CytokineReceptors, Interleukin-18Receptors, Interleukin-1 Type IIReceptors, Pattern RecognitionRespiratory Syncytial VirusesRespiratory Syncytial Virus InfectionsRespiratory Tract InfectionsSignal TransductionAdaptor Proteins, Signal TransducingAdaptor Proteins, Vesicular TransportIL1R2 protein, humanMAVS protein, mouseMyd88 protein, mouseMyeloid Differentiation Factor 88Receptors, CytokineReceptors, Interleukin-18Receptors, Interleukin-1 Type IIReceptors, Pattern RecognitionTicam1 protein, mouse

Identifiers

PMID26688048
PMCPMC4685246
OpenAlexW2401427917

What OpenQuestion holds

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LicenceCC BY
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.