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

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

2016
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Overview
The function of group 3 innate lymphoid cells (ILC3 cells) is still being determined. Vivier and colleagues describe the development of ILC3 subsets and show that NCR + ILC3 cells are not needed to control infection with Citrobacter rodentium in the presence of an intact T cell compartment. 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.