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.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Niedbala W,Besnard AG,Nascimento DC,Donate PB,Sonego F,Yip E,Guabiraba R,Chang HD,Fukada SY,Salmond RJ,Schmitt E,Bopp T,Ryffel B,Liew FYdoi
10.1038/ncomms5575subject
Has Abstractpub_date
2014-08-07 00:00:00pages
4575issn
2041-1723pii
ncomms5575journal_volume
5pub_type
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