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Nat Immunol. 2016 Jan;17(1):76-86. doi: 10.1038/ni.3309. Epub 2015 Nov 23.

Interferon and IL-27 antagonize the function of group 2 innate lymphoid cells and type 2 innate immune responses.

Author information

1
Laboratory for Immune Cell Systems, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
2
Laboratory for Innate Immune Systems, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
3
Precursory Research for Embryonic Science and Technology, Japan Science and Technology Agency, Tokyo, Japan.
4
Division of Immunobiology, Department of Medical Life Science, Graduate School of Medical Life Science, Yokohama City University, Yokohama, Japan.
5
Division of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
6
Department of Infectious Diseases, Keio University School of Medicine, Tokyo, Japan.
7
Division of Pulmonary Medicine, Department of Medicine, Tokai University School of Medicine, Kanagawa, Japan.
8
Department of Microbiology and Immunology, Keio University School of Medicine, Tokyo, Japan.

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 TH2 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.

PMID:
26595888
DOI:
10.1038/ni.3309
[Indexed for MEDLINE]

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