Type I interferon restricts type 2 immunopathology through the regulation of group 2 innate lymphoid cells

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

Research output: Contribution to journalArticlepeer-review

282 Scopus citations

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.

Original languageEnglish
Pages (from-to)65-75
Number of pages11
JournalNature Immunology
Volume17
Issue number1
DOIs
StatePublished - Jan 1 2016
Externally publishedYes

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