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

被引:199
|
作者
Rankin, Lucille C. [1 ,2 ,17 ]
Girard-Madoux, Mathilde J. H. [3 ]
Seillet, Cyril [1 ,2 ]
Mielke, Lisa A. [1 ,2 ]
Kerdiles, Yann [3 ]
Fenis, Aurore [3 ]
Wieduwild, Elisabeth [3 ]
Putoczki, Tracy [1 ,2 ]
Mondot, Stanislas [4 ]
Lantz, Olivier [5 ,6 ]
Demon, Dieter [7 ,8 ]
Papenfuss, Anthony T. [1 ,2 ]
Smyth, Gordon K. [1 ,2 ,9 ]
Lamkanfi, Mohamed [7 ,8 ]
Carotta, Sebastian [1 ,2 ,10 ]
Renauld, Jean-Christophe [11 ,12 ]
Shi, Wei [1 ,2 ,13 ]
Carpentier, Sabrina [14 ]
Soos, Tim [15 ]
Arendt, Christopher
Ugolini, Sophie [3 ]
Huntington, Nicholas D. [1 ,2 ]
Bez, Gabrielle T. [1 ,2 ]
Vivier, Eric [1 ,3 ,16 ]
机构
[1] Univ Melbourne, Walter & Eliza Hall Inst Med Res, Parkville, Vic 3052, Australia
[2] Univ Melbourne, Dept Med Biol, Parkville, Vic 3052, Australia
[3] Univ Aix Marseille, Ctr Immunol Marseille Luminy, CNRS, Inserm,U1104,UMR7280,UM2, Marseille, France
[4] Inst Pasteur, Labex Milieu Interieur, Paris, France
[5] Inst Curie, Lab Immunol, Paris, France
[6] Inst Curie, INSERM, U932, Paris, France
[7] Univ Ghent, VIB, Inflammat Res Ctr, B-9000 Ghent, Belgium
[8] Univ Ghent, Dept Biochem, B-9000 Ghent, Belgium
[9] Univ Melbourne, Dept Math & Stat, Parkville, Vic 3052, Australia
[10] Boehringer Ingelheim RCV, Vienna, Austria
[11] Catholic Univ Louvain, Ludwig Inst Canc Res, Brussels, Belgium
[12] Catholic Univ Louvain, Expt Med Unit, Brussels, Belgium
[13] Univ Melbourne, Dept Comp & Informat Syst, Parkville, Vic 3052, Australia
[14] Aix Marseille Univ, MI mAbs Consortium, Ctr Immunol Marseille Luminy, Marseille, France
[15] SANOFI, Bioinnovat, Boston, MA USA
[16] Hop Conception, AP HP, Immunol, Marseille, France
[17] Cornell Univ, Weill Cornell Med Coll, New York, NY 10021 USA
基金
英国医学研究理事会; 欧洲研究理事会; 澳大利亚研究理事会;
关键词
NATURAL-KILLER-CELLS; NK CELLS; T-CELL; COMMENSAL BACTERIA; IL-22; PRODUCTION; HOST-DEFENSE; INTERLEUKIN-22; INFLAMMATION; LYMPHOCYTES; INFECTION;
D O I
10.1038/ni.3332
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:179 / 186
页数:8
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