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

0494339 - ÚMG 2019 RIV US eng J - Článek v odborném periodiku
Burrows, K. - Antignano, F. - Chenery, A. - Bramhall, M. - Kořínek, Vladimír - Underhill, T. M. - Zaph, C.
HIC1 links retinoic acid signalling to group 3 innate lymphoid cell-dependent regulation of intestinal immunity and homeostasis.
PLoS Pathogens. Roč. 14, č. 2 (2018), č. článku e1006869. ISSN 1553-7366. E-ISSN 1553-7374
Institucionální podpora: RVO:68378050
Klíčová slova: cd103(+)cd11b(+) dendritic cells * t-cells * transcription factors * foxp3 induction * nkp46(+) cells * differentiation * inflammation * expression * defense * gut
Obor OECD: Biochemistry and molecular biology
Impakt faktor: 6.463, rok: 2018

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.
Trvalý link: http://hdl.handle.net/11104/0287567