Evidence map›Paper›PMID 25099390›Full record

ArticleNature communications2014

Nitric oxide enhances Th9 cell differentiation and airway inflammation.

Wanda Niedbala, Anne-Gaelle Besnard, Daniele Carvalho Nascimento, Paula Barbim Donate, Fabiane Sonego, Edwin Yip, Rodrigo Guabiraba, Hyun-Dong Chang, Sandra Y Fukada, Robert J Salmond and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.2field-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.

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

30 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
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  6. T cells in health and disease.Signal transduction and targeted therapy · 2023
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  11. Review
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  13. B lymphocyte-induced maturation protein 1 controls TThe Journal of allergy and clinical immunology · 2019
    Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. TSeminars in immunopathology · 2017
    Review
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

14 authors at 6 institutions in 5 countries.

Wanda NiedbalaDepartment of Immunology, Institute of Infection, Immunity and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow, Glasgow G12 8TA, UK.
Anne-Gaelle BesnardDepartment of Immunology, Institute of Infection, Immunity and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow, Glasgow G12 8TA, UK.
Daniele Carvalho Nascimento1] Department of Immunology, Institute of Infection, Immunity and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow, Glasgow G12 8TA, UK [2] Inflammation and Pain Group, Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo 14049-900, Brazil.
Paula Barbim DonateInflammation and Pain Group, Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo 14049-900, Brazil.
Fabiane SonegoDepartment of Immunology, Institute of Infection, Immunity and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow, Glasgow G12 8TA, UK.
Edwin YipDepartment of Immunology, Institute of Infection, Immunity and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow, Glasgow G12 8TA, UK.
Rodrigo GuabirabaDepartment of Immunology, Institute of Infection, Immunity and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow, Glasgow G12 8TA, UK.
Hyun-Dong ChangCell Biology Group, German Rheumatism Research Center, a Leibniz Institute, 10117 Berlin, Germany.
Sandra Y FukadaDepartment of Immunology, Institute of Infection, Immunity and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow, Glasgow G12 8TA, UK.
Robert J SalmondDepartment of Immunology, Institute of Infection, Immunity and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow, Glasgow G12 8TA, UK.
Edgar SchmittInstitute for Immunology, University Medical Centre, Johannes Gutenberg University Mainz, D55131 Mainz, Germany.
Tobias BoppInstitute for Immunology, University Medical Centre, Johannes Gutenberg University Mainz, D55131 Mainz, Germany.
Bernhard Ryffel1] University of Orleans and CNRS UMR7355, Transgenose Institute, 45071 Orleans, France [2] Institute of Infectious Disease and Molecular Medicine (IIDMM), University of Cape Town, 7700 Rondebosch, RSA.
Foo Y Liew1] Department of Immunology, Institute of Infection, Immunity and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow, Glasgow G12 8TA, UK [2] CEGMR, King Abdul-Aziz University, Jeddah 21589, Kingdom of Saudi Arabia [3] School of Biological &Basic Medical Science, Soochow University, Suzhou 215006, China.
University of Glasgow · GBHospital Universitário da Universidade de São Paulo · BRJohannes Gutenberg University Mainz · DEImmunologie et Neurogénétique Expérimentales et Moléculaires · FRKing Abdulaziz University · SALeibniz Association · DE

Funding

Medical Research Council G9818261Wellcome Trust 080217
6 · The paper itself

Abstract

Th9 cells protect hosts against helminthic infection but also mediate allergic disease. Here we show that nitric oxide (NO) promotes Th9 cell polarization of murine and human CD4(+) T cells. NO de-represses the tumour suppressor gene p53 via nitrosylation of Mdm2. NO also increases p53-mediated IL-2 production, STAT5 phosphorylation and IRF4 expression, all essential for Th9 polarization. NO also increases the expression of TGFβR and IL-4R, pivotal to Th9 polarization. OVA-sensitized mice treated with an NO donor developed more severe airway inflammation. Transferred Th9 cells induced airway inflammation, which was exacerbated by NO and blocked by anti-IL-9 antibody. Nos2(-/-) mice had less Th9 cells and developed attenuated eosinophilia during OVA-induced airway inflammation compared with wild-type mice. Our data demonstrate that NO is an important endogenous inducer of Th9 cells and provide a hitherto unrecognized mechanism for NO-mediated airway inflammation via the expansion of Th9 cells.

Indexed as

Cell DifferentiationAnimalsCD4-Positive T-LymphocytesCells, CulturedCell SeparationEosinophiliaFlow CytometryHumansInflammationInterferon Regulatory Factor-4Interferon Regulatory FactorsInterleukin-2Interleukin-9Leukocytes, MononuclearMiceMice, Inbred BALB CInterferon Regulatory Factor-4Interferon Regulatory FactorsInterleukin-2Interleukin-9Nitric OxideNitric Oxide Synthase Type IINOS2 protein, humanNos2 protein, mouseSTAT5 Transcription FactorTumor Suppressor Protein p53

Identifiers

PMID25099390
PMCPMC4131005
OpenAlexW2050339985

What OpenQuestion holds

Textmetadata
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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.