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Duerr CU , McCarthy CD , Mindt BC , Rubio M , Meli AP , Pothlichet J , Eva MM , Gauchat JF , Qureshi ST , Mazer BD , Mossman KL , Malo D , Gamero AM , Vidal SM , King IL , Sarfati M , Fritz JH
Type I interferon restricts type 2 immunopathology through the regulation of group 2 innate lymphoid cells
Nat Immunol. 2016 Nov 23;17(1) :65-75
PMID: 26595887 URL: http://www.ncbi.nlm.nih.gov/pubmed/26595887
AbstractViral 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.
NotesDuerr, Claudia U McCarthy, Connor D A Mindt, Barbara C Rubio, Manuel Meli, Alexandre P Pothlichet, Julien Eva, Megan M Gauchat, Jean-Francois Qureshi, Salman T Mazer, Bruce D Mossman, Karen L Malo, Danielle Gamero, Ana M Vidal, Silvia M King, Irah L Sarfati, Marika Fritz, Jorg H Nat Immunol. 2015 Nov 23. doi: 10.1038/ni.3308.