期刊
NATURE IMMUNOLOGY
卷 17, 期 2, 页码 179-186出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.3332
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资金
- National Health and Medical Research Council of Australia
- Dora Lush Postgraduate Research Scholarship
- Australian Research Council
- Victorian State Government Operational Infrastructure Support
- Australian Government National Health and Medical Research Council Independent Research Institutes Infrustructure Support
- European Research Council (THINK Advanced Grant)
- Ligue Nationale contre le Cancer (Equipe Labellisee)
- INSERM
- CNRS
- Aix-Marseille University
- Institut Universitaire de France
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, 1122, 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.
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