@article{f3cb094db70b47749af16308cf9c0663,
title = "Interferon and IL-27 antagonize the function of group 2 innate lymphoid cells and type 2 innate immune responses",
abstract = "Group 2 innate lymphoid cells (ILC2 cells) are type 2 cytokine-producing cells of the innate immune system with important roles in helminth infection and allergic inflammation. Here we found that tissue-resident ILC2 cells proliferated in situ without migrating during inflammatory responses. Both type I and type II interferons and interleukin 27 (IL-27) suppressed ILC2 function in a manner dependent on the transcription factor STAT1. ILC2-mediated lung inflammation was enhanced in the absence of the interferon-γ (IFN-γ) receptor on ILC2 cells in vivo. IFN-γ effectively suppressed the function of tissue-resident ILC2 cells but not that of inflammatory ILC2 cells, and IL-27 suppressed tissue-resident ILC2 cells but not tissue-resident T H 2 cells during lung inflammation induced by Alternaria alternata. Our results demonstrate that suppression mediated by interferon and IL-27 is a negative feedback mechanism for ILC2 function in vivo.",
author = "Kazuyo Moro and Hiroki Kabata and Masanobu Tanabe and Satoshi Koga and Natsuki Takeno and Miho Mochizuki and Koichi Fukunaga and Koichiro Asano and Tomoko Betsuyaku and Shigeo Koyasu",
note = "Funding Information: We thank M. Kubo (Tokyo University of Science) for IfngVenus/+ mice; M. Miyasaka (Osaka University) for antibody to mouse IL-2Rβ (TM-β1); S. Wada, T. Yamamoto, T. Shitamichi, U. Tran and S. Tada for animal care; M. Yamamoto, S. Kagawa, T. Fukushima and J. Furusawa for help in some experiments; Kafi N. Ealey for critical reading of this manuscript; and members of the Laboratory for Immune Cell Systems at RIKEN Integrative Medical Sciences for discussion. Supported by Precursory Research for Embryonic Science and Technology from Japan Science and Technology Agency Japan Society for the Promotion of Science (Grant-in Aid for Scientific Research (B) 26293110; Grant-in-Aid for Challenging Exploratory Research 24659373 to K.M.; Grant-in-Aid for Scientific Research (S) 22229004 to S.K.) and the Ministry of Education, Culture, Sports, Science and Technology of Japan (Grant-in-Aid for Scientific Research on Innovative Areas 15H01166 to K.M.). Publisher Copyright: {\textcopyright} 2016 Nature America, Inc.",
year = "2016",
month = jan,
day = "1",
doi = "10.1038/ni.3309",
language = "English",
volume = "17",
pages = "76--86",
journal = "Nature Immunology",
issn = "1529-2908",
publisher = "Nature Publishing Group",
number = "1",
}