HIC1 links retinoic acid signalling to group 3 innate lymphoid cell-dependent regulation of intestinal immunity and homeostasis

PLoS Pathogens
Kyle BurrowsColby Zaph

Abstract

The intestinal immune system must be able to respond to a wide variety of infectious organisms while maintaining tolerance to non-pathogenic microbes and food antigens. The Vitamin A metabolite all-trans-retinoic acid (atRA) has been implicated in the regulation of this balance, partially by regulating innate lymphoid cell (ILC) responses in the intestine. However, the molecular mechanisms of atRA-dependent intestinal immunity and homeostasis remain elusive. Here we define a role for the transcriptional repressor Hypermethylated in cancer 1 (HIC1, ZBTB29) in the regulation of ILC responses in the intestine. Intestinal ILCs express HIC1 in a vitamin A-dependent manner. In the absence of HIC1, group 3 ILCs (ILC3s) that produce IL-22 are lost, resulting in increased susceptibility to infection with the bacterial pathogen Citrobacter rodentium. Thus, atRA-dependent expression of HIC1 in ILC3s regulates intestinal homeostasis and protective immunity.

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Citations

Feb 21, 2019·Investigative Ophthalmology & Visual Science·Justin Ma, Peter Lwigale
Feb 7, 2020·Cells·Marion Rolot, Timothy E O'Sullivan
Jun 11, 2020·Annual Review of Nutrition·Samuel Philip NobsEran Elinav
Sep 6, 2020·Microorganisms·Katharina BeckNaoko Satoh-Takayama
May 18, 2021·Frontiers in Immunology·Zhengzheng ShiNaoko Satoh-Takayama
Aug 20, 2021·Mucosal Immunology·Aidil Zaini, Colby Zaph

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Methods Mentioned

BETA
flow cytometry
PCR

Software Mentioned

FlowJo
TreeStar
GraphPad Prism

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