| First Author | Burrows K | Year | 2018 |
| Journal | PLoS Pathog | Volume | 14 |
| Issue | 2 | Pages | e1006869 |
| PubMed ID | 29470558 | Mgi Jnum | J:277542 |
| Mgi Id | MGI:6296192 | Doi | 10.1371/journal.ppat.1006869 |
| Citation | Burrows K, et al. (2018) HIC1 links retinoic acid signalling to group 3 innate lymphoid cell-dependent regulation of intestinal immunity and homeostasis. PLoS Pathog 14(2):e1006869 |
| abstractText | 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. |
