Complementarity and redundancy of IL-22-producing innate lymphoid cells
- Author(s)
- Rankin, LC; Girard-Madoux, MJ; Seillet, C; Mielke, LA; Kerdiles, Y; Fenis, A; Wieduwild, E; Putoczki, T; Mondot, S; Lantz, O; Demon, D; Papenfuss, AT; Smyth, GK; Lamkanfi, M; Carotta, S; RENAULD, JC; Shi, W; Carpentier, S; Soos, T; Arendt, C; Ugolini, S; Huntington, ND; Belz, GT; Vivier, E;
- Details
- Publication Year 2016-02,Volume 17,Issue #2,Page 179-186
- Journal Title
- Nat Immunol
- Publication Type
- Journal Article
- 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.
- Publisher
- NPG
- Research Division(s)
- Molecular Immunology; Inflammation; Bioinformatics
- PubMed ID
- 26595889
- Link To PubMed Central Version
- https://www-ncbi-nlm-nih-govpmc/articles/PMC4720992/
- Publisher's Version
- https://doi.org/10.1038/ni.3332
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2015-12-10 11:27:51
Last Modified: 2018-01-09 12:59:14