Author
Listed:
- Wanda Niedbala
(Institute of Infection, Immunity and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow)
- Anne-Gaelle Besnard
(Institute of Infection, Immunity and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow)
- Daniele Carvalho Nascimento
(Institute of Infection, Immunity and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow
Inflammation and Pain Group, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto)
- Paula Barbim Donate
(Inflammation and Pain Group, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto)
- Fabiane Sonego
(Institute of Infection, Immunity and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow)
- Edwin Yip
(Institute of Infection, Immunity and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow)
- Rodrigo Guabiraba
(Institute of Infection, Immunity and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow)
- Hyun-Dong Chang
(Cell Biology Group, German Rheumatism Research Center, a Leibniz Institute)
- Sandra Y. Fukada
(Institute of Infection, Immunity and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow)
- Robert J. Salmond
(Institute of Infection, Immunity and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow)
- Edgar Schmitt
(Institute for Immunology, University Medical Centre, Johannes Gutenberg University Mainz)
- Tobias Bopp
(Institute for Immunology, University Medical Centre, Johannes Gutenberg University Mainz)
- Bernhard Ryffel
(University of Orleans and CNRS UMR7355, Transgenose Institute
Institute of Infectious Disease and Molecular Medicine (IIDMM), University of Cape Town)
- Foo Y. Liew
(Institute of Infection, Immunity and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow
CEGMR, King Abdul-Aziz University
School of Biological & Basic Medical Science, Soochow University)
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.
Suggested Citation
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 & Edg, 2014.
"Nitric oxide enhances Th9 cell differentiation and airway inflammation,"
Nature Communications, Nature, vol. 5(1), pages 1-13, December.
Handle:
RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5575
DOI: 10.1038/ncomms5575
Download full text from publisher
Corrections
All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5575. See general information about how to correct material in RePEc.
If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.
We have no bibliographic references for this item. You can help adding them by using this form .
If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.
For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .
Please note that corrections may take a couple of weeks to filter through
the various RePEc services.