| First Author | Duerr CU | Year | 2016 |
| Journal | Nat Immunol | Volume | 17 |
| Issue | 1 | Pages | 65-75 |
| PubMed ID | 26595887 | Mgi Jnum | J:234573 |
| Mgi Id | MGI:5790281 | Doi | 10.1038/ni.3308 |
| Citation | Duerr CU, et al. (2016) Type I interferon restricts type 2 immunopathology through the regulation of group 2 innate lymphoid cells. Nat Immunol 17(1):65-75 |
| abstractText | 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. |
