Complementarity and redundancy of IL-22-producing innate lymphoid cells View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-02

AUTHORS

Lucille C Rankin, Mathilde J H Girard-Madoux, Cyril Seillet, Lisa A Mielke, Yann Kerdiles, Aurore Fenis, Elisabeth Wieduwild, Tracy Putoczki, Stanislas Mondot, Olivier Lantz, Dieter Demon, Anthony T Papenfuss, Gordon K Smyth, Mohamed Lamkanfi, Sebastian Carotta, Jean-Christophe Renauld, Wei Shi, Sabrina Carpentier, Tim Soos, Christopher Arendt, Sophie Ugolini, Nicholas D Huntington, Gabrielle T Belz, Eric Vivier

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. More... »

PAGES

179-186

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ni.3332

DOI

http://dx.doi.org/10.1038/ni.3332

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1047264989

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/26595889


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