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- W2216745061 abstract "Viral respiratory tract infections are the main causative agents of the onset of infection-induced asthma and asthma exacerbations that remain mechanistically unexplained. Here we found that deficiency in signaling via type I interferon receptor led to deregulated activation of group 2 innate lymphoid cells (ILC2 cells) and infection-associated type 2 immunopathology. Type I interferons directly and negatively regulated mouse and human ILC2 cells in a manner dependent on the transcriptional activator ISGF3 that led to altered cytokine production, cell proliferation and increased cell death. In addition, interferon-γ (IFN-γ) and interleukin 27 (IL-27) altered ILC2 function dependent on the transcription factor STAT1. These results demonstrate that type I and type II interferons, together with IL-27, regulate ILC2 cells to restrict type 2 immunopathology." @default.
- W2216745061 created "2016-06-24" @default.
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- W2216745061 date "2015-11-23" @default.
- W2216745061 modified "2023-10-01" @default.
- W2216745061 title "Type I interferon restricts type 2 immunopathology through the regulation of group 2 innate lymphoid cells" @default.
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- W2216745061 doi "https://doi.org/10.1038/ni.3308" @default.
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