Type I interferon restricts type 2 immunopathology through the regulation of group 2 innate lymphoid cells Academic Article uri icon

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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.

authors

  • Duerr, Claudia U
  • McCarthy, Connor DA
  • Mindt, Barbara C
  • Rubio, Manuel
  • Meli, Alexandre P
  • Pothlichet, Julien
  • Eva, Megan M
  • Gauchat, Jean-François
  • Qureshi, Salman T
  • Mazer, Bruce D
  • Mossman, Karen
  • Malo, Danielle
  • Gamero, Ana M
  • Vidal, Silvia M
  • King, Irah L
  • Sarfati, Marika
  • Fritz, Jörg H

publication date

  • January 2016