Evidence map›Paper›PMID 31780735›Full record

ArticleScientific reports2019

Respiratory syncytial virus reduces STAT3 phosphorylation in human memory CD8 T cells stimulated with IL-21.

Krist Helen Antunes, André Becker, Caroline Franceschina, Deise do Nascimento de Freitas, Isadora Lape, Mariana D'Ávila da Cunha, Lidiane Leitão, Mauricio M Rigo, Leonardo Araújo Pinto, Renato T Stein and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

7 citing papers in PubMed, 7 citations in OpenAlex.

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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

11 authors at 2 institutions in 1 country.

Krist Helen AntunesLaboratory of Clinical and experimental Immunology, Infant Center, School of Medicine, Pontificia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil.ORCID http://orcid.org/0000-0002-1525-6581
André BeckerLaboratory of Clinical and experimental Immunology, Infant Center, School of Medicine, Pontificia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil.
Caroline FranceschinaLaboratory of Clinical and experimental Immunology, Infant Center, School of Medicine, Pontificia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil.
Deise do Nascimento de FreitasLaboratory of Clinical and experimental Immunology, Infant Center, School of Medicine, Pontificia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil.
Isadora LapeLaboratory of Clinical and experimental Immunology, Infant Center, School of Medicine, Pontificia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil.
Mariana D'Ávila da CunhaLaboratory of Clinical and experimental Immunology, Infant Center, School of Medicine, Pontificia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil.
Lidiane LeitãoLaboratory of Respiratory Physiology, Infant Center, School of Medicine, PUCRS, Porto Alegre, Brazil.
Mauricio M RigoLaboratory of Clinical and experimental Immunology, Infant Center, School of Medicine, Pontificia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil.
Leonardo Araújo PintoLaboratory of Respiratory Physiology, Infant Center, School of Medicine, PUCRS, Porto Alegre, Brazil.ORCID http://orcid.org/0000-0002-3906-5456
Renato T SteinLaboratory of Respiratory Physiology, Infant Center, School of Medicine, PUCRS, Porto Alegre, Brazil.
Ana Paula Duarte de SouzaLaboratory of Clinical and experimental Immunology, Infant Center, School of Medicine, Pontificia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil. ana.duarte@pucrs.br.ORCID http://orcid.org/0000-0002-6021-5068
Pontifícia Universidade Católica do Rio Grande do Sul · BRHospital São Lucas da PUCRS · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Respiratory syncytial virus (RSV) is a common cause of childhood lower respiratory tract infections. The recent failure of a vaccine candidate based on recombinant F protein underlines the urgent need to better understand the protective human memory immune response against RSV. Signal transducer and activator of transcription 3 (STAT3) protein is a transcription factor that promotes the maturation of the memory CD8 T cell response in cooperation with IL-10 and IL-21. However, the role of STAT3 in the memory CD8 T cell response during RSV infection remains to be elucidated. We found that in infants with bronchiolitis infected with RSV, the expression of STAT3 detected in nasal washes is reduced when compared to that in infants infected by other viruses. In vitro, RSV impairs STAT3 phosphorylation induced by IL-21 in purified human memory CD8 T cells. In addition, RSV decreases granzyme B production by memory CD8 T cells, reducing its cytotoxic activity against RSV-infected epithelial pulmonary cell lines. Together, these data indicate that RSV modulates the IL-21/STAT3 pathway in human memory CD8 T cells, and this could be a mechanism to be further explored to improve the memory response against the infection.

Indexed as

CD8-Positive T-LymphocytesCells, CulturedFemaleHost-Pathogen InteractionsHumansImmunologic MemoryInfantInterleukin-21InterleukinsMaleModels, MolecularPhosphorylationRespiratory Syncytial Virus, HumanRespiratory Syncytial Virus InfectionsSTAT3 Transcription FactorInterleukin-21InterleukinsSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID31780735
PMCPMC6882881
OpenAlexW2989597030

What OpenQuestion holds

Textmetadata
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.