Evidence map›Paper›PMID 26037291›Full record

ArticleBMC immunology2015

Murine IL-17+ Vγ4 T lymphocytes accumulate in the lungs and play a protective role during severe sepsis.

Maria Fernanda de Souza Costa, Catarina Bastos Trigo de Negreiros, Victor Ugarte Bornstein, Richard Hemmi Valente, José Mengel, Maria das Graças Henriques, Claudia Farias Benjamim, Carmen Penido

Open access · goldAbstract read
In one paragraph

Article in BMC immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 35 citations in OpenAlex.

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  14. Innate T cells in the intensive care unit.Molecular immunology · 2019
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  20. Genetic variation in chromosome Y regulates susceptibility to influenza A virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2017
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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

8 authors at 4 institutions in 2 countries.

Maria Fernanda de Souza CostaLaboratório de Farmacologia Aplicada, Departamento de Farmacologia, Farmanguinhos, Fundação Oswaldo Cruz, Rua Sizenando Nabuco 100, Manguinhos, Rio de Janeiro, RJ, CEP 21041-250, Brazil. mfcosta@cdts.fiocruz.br.
Catarina Bastos Trigo de NegreirosLaboratório de Farmacologia Aplicada, Departamento de Farmacologia, Farmanguinhos, Fundação Oswaldo Cruz, Rua Sizenando Nabuco 100, Manguinhos, Rio de Janeiro, RJ, CEP 21041-250, Brazil. catarinanegreiros@far.fiocruz.br.
Victor Ugarte BornsteinLaboratório de Farmacologia Aplicada, Departamento de Farmacologia, Farmanguinhos, Fundação Oswaldo Cruz, Rua Sizenando Nabuco 100, Manguinhos, Rio de Janeiro, RJ, CEP 21041-250, Brazil. victo.bornstein@mssm.edu.
Richard Hemmi ValenteLaboratório de Toxinologia, Instituto Oswaldo Cruz, Fundação Oswaldo Cruz, Rio de Janeiro, Brazil. rhv4u@ioc.fiocruz.br.
José MengelLaboratório de Imunologia, Faculdade de Medicina de Petrópolis, Petrópolis, Rio de Janeiro, Brazil. jomengel@fiocruz.br.
Maria das Graças HenriquesLaboratório de Farmacologia Aplicada, Departamento de Farmacologia, Farmanguinhos, Fundação Oswaldo Cruz, Rua Sizenando Nabuco 100, Manguinhos, Rio de Janeiro, RJ, CEP 21041-250, Brazil. gracahenriques@fiocruz.br.
Claudia Farias BenjamimLaboratório de Inflamação, Estresse Oxidativo e Câncer, Centro de Ciências da Saúde, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil. cbenjamim@icb.ufrj.br.
Carmen PenidoLaboratório de Farmacologia Aplicada, Departamento de Farmacologia, Farmanguinhos, Fundação Oswaldo Cruz, Rua Sizenando Nabuco 100, Manguinhos, Rio de Janeiro, RJ, CEP 21041-250, Brazil. cpenido@cdts.fiocruz.br.
Fundação Oswaldo Cruz · BRFaculdade de Medicina de Petrópolis · BRMount Sinai Hospital · USUniversidade Federal do Rio de Janeiro · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLung inflammation is a major consequence of the systemic inflammatory response caused by severe sepsis. Increased migration of γδ T lymphocytes into the lungs has been previously demonstrated during experimental sepsis; however, the involvement of the γδ T cell subtype Vγ4 has not been previously described.

methodsSevere sepsis was induced by cecal ligation and puncture (CLP; 9 punctures, 21G needle) in male C57BL/6 mice. γδ and Vγ4 T lymphocyte depletion was performed by 3A10 and UC3-10A6 mAb i.p. administration, respectively. Lung infiltrating T lymphocytes, IL-17 production and mortality rate were evaluated.

resultsSevere sepsis induced by CLP in C57BL/6 mice led to an intense lung inflammatory response, marked by the accumulation of γδ T lymphocytes (comprising the Vγ4 subtype). γδ T lymphocytes present in the lungs of CLP mice were likely to be originated from peripheral lymphoid organs and migrated towards CCL2, CCL3 and CCL5, which were highly produced in response to CLP-induced sepsis. Increased expression of CD25 by Vγ4 T lymphocytes was observed in spleen earlier than that by αβ T cells, suggesting the early activation of Vγ4 T cells. The Vγ4 T lymphocyte subset predominated among the IL-17(+) cell populations present in the lungs of CLP mice (unlike Vγ1 and αβ T lymphocytes) and was strongly biased toward IL-17 rather than toward IFN-γ production. Accordingly, the in vivo administration of anti-Vγ4 mAb abrogated CLP-induced IL-17 production in mouse lungs. Furthermore, anti-Vγ4 mAb treatment accelerated mortality rate in severe septic mice, demonstrating that Vγ4 T lymphocyte play a beneficial role in host defense.

conclusionsOverall, our findings provide evidence that early-activated Vγ4 T lymphocytes are the main responsible cells for IL-17 production in inflamed lungs during the course of sepsis and delay mortality of septic mice.

Indexed as

AnimalsAntibodies, MonoclonalCecumCell MovementChemokinesInterleukin-17LigationLungLymphocyte ActivationMaleMice, Inbred C57BLProtective AgentsPuncturesReceptors, Antigen, T-Cell, gamma-deltaSepsisSpleenAntibodies, MonoclonalChemokinesInterleukin-17Protective AgentsReceptors, Antigen, T-Cell, gamma-delta

Identifiers

PMID26037291
PMCPMC4451961
OpenAlexW1847094188

What OpenQuestion holds

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LicenceCC BY
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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.