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Duerr, Claudia U; McCarthy, Connor D A; Mindt, Barbara C; Rubio, Manuel; Meli, Alexandre P; Pothlichet, Julien; Eva, Megan M; Gauchat, Jean-François; Qureshi, Salman T; Mazer, Bruce D; Mossman, Karen L; Malo, Danielle; Gamero, Ana M; Vidal, Silvia M; King, Irah L; Sarfati, Marika; Fritz, Jörg H
Nature immunology, 01/2016, Volume: 17, Issue: 1Journal Article
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.
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