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- W2050339985 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. Th9 cells are a subset of T helper cells that protect hosts against helminthic infection, but can also mediate allergic disease through overexpression of the cytokine IL-9. Here, Niedbala et al.show that nitric oxide is a potent enhancer of Th9 differentiation via the activation of p53 protein." @default.
- W2050339985 created "2016-06-24" @default.
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- W2050339985 date "2014-08-07" @default.
- W2050339985 modified "2023-10-18" @default.
- W2050339985 title "Nitric oxide enhances Th9 cell differentiation and airway inflammation" @default.
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- W2050339985 doi "https://doi.org/10.1038/ncomms5575" @default.
- W2050339985 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4131005" @default.
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- W2050339985 hasPublicationYear "2014" @default.
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