Format

Send to

Choose Destination
Nat Immunol. 2016 Feb;17(2):179-86. doi: 10.1038/ni.3332. Epub 2015 Nov 30.

Complementarity and redundancy of IL-22-producing innate lymphoid cells.

Author information

1
The Walter and Eliza Hall Institute of Medical Research, and Department of Medical Biology, University of Melbourne, Parkville, Australia.
2
Department of Medical Biology, University of Melbourne, Parkville, Australia.
3
Centre d'Immunologie de Marseille-Luminy, Université d'Aix-Marseille UM2, Inserm, U1104, CNRS UMR7280, Marseille, France.
4
Labex Milieu Intérieur, Institut Pasteur, Paris, France.
5
Laboratoire d'Immunologie and Inserm U932, Institut Curie, Paris, France.
6
Inflammation Research Center, VIB, Ghent University, Ghent, Belgium.
7
Department of Biochemistry, Ghent University, Ghent, Belgium.
8
Department of Mathematics and Statistics, University of Melbourne, Parkville, Australia.
9
Boehringer-Ingelheim RCV, Vienna, Austria.
10
Ludwig Institute for Cancer Research and Experimental Medicine Unit, Catholic University of Louvain, Brussels, Belgium.
11
Department of Computing and Information Systems, University of Melbourne, Parkville, Australia.
12
MI-mAbs consortium Aix-Marseille University, Centre d'Immunologie de Marseille-Luminy, Marseille, France.
13
Bioinnovation, SANOFI, Boston, Massachusetts, USA.
14
Immunologie, Hôpital de la Conception, Assistance Publique-Hôpitaux de Marseille, Marseille, France.

Abstract

Intestinal T cells and group 3 innate lymphoid cells (ILC3 cells) control the composition of the microbiota and gut immune responses. Within the gut, ILC3 subsets coexist that either express or lack the natural cytoxicity receptor (NCR) NKp46. We identified here the transcriptional signature associated with the transcription factor T-bet-dependent differentiation of NCR(-) ILC3 cells into NCR(+) ILC3 cells. Contrary to the prevailing view, we found by conditional deletion of the key ILC3 genes Stat3, Il22, Tbx21 and Mcl1 that NCR(+) ILC3 cells were redundant for the control of mouse colonic infection with Citrobacter rodentium in the presence of T cells. However, NCR(+) ILC3 cells were essential for cecal homeostasis. Our data show that interplay between intestinal ILC3 cells and adaptive lymphocytes results in robust complementary failsafe mechanisms that ensure gut homeostasis.

PMID:
26595889
PMCID:
PMC4720992
DOI:
10.1038/ni.3332
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center