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

By Kyle Burrows, Frann Antignano, Alistair Chenery, Vladimir Korinek, T. Michael Underhill, Colby Zaph

Posted 13 Feb 2017
bioRxiv DOI: 10.1101/108241 (published DOI: 10.1371/journal.ppat.1006869)

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 retinoic acid (RA) 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 RA-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 ana vitamin A-dependent manner. In the absence of HIC1, group 3 ILCs (ILC3s) are lost, resulting in increased susceptibility to infection with the bacterial pathogen Citrobacter rodentium. In addition, the loss of ILC3s leads to a local and systemic increase in IFN-γ-producing T cells that prevents the development of protective immunity against infection with the parasitic helminth Trichuris muris. Thus, RA-dependent expression of HIC1 in ILC3s regulates intestinal homeostasis and protective immunity.

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