Journal
NATURE IMMUNOLOGY
Volume 17, Issue 1, Pages 65-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.3308
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Funding
- Canadian Institutes of Health Research [MOP-114972, MOP-89821]
- Canadian Foundation of Innovation
- German National Academy of Sciences Leopoldina
- American Association of Immunologists Careers in Immunology Fellowship Program
- Canada Research Chair in Host Responses to Virus Infections
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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-gamma (IFN-gamma) 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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