| Literature DB >> 30397350 |
Giovanni A M Povoleri1,2, Estefania Nova-Lamperti1,2, Cristiano Scottà1,2, Giorgia Fanelli1,2, Yun-Ching Chen3, Pablo D Becker1,2, Dominic Boardman1,2, Benedetta Costantini4, Marco Romano1,2, Polychronis Pavlidis1,2, Reuben McGregor1,2, Eirini Pantazi1,2, Daniel Chauss5, Hong-Wei Sun6, Han-Yu Shih7, David J Cousins8, Nichola Cooper9, Nick Powell1,2, Claudia Kemper10, Mehdi Pirooznia3, Arian Laurence11, Shahram Kordasti4, Majid Kazemian12, Giovanna Lombardi1,2, Behdad Afzali13,14,15.
Abstract
Repair of tissue damaged during inflammatory processes is key to the return of local homeostasis and restoration of epithelial integrity. Here we describe CD161+ regulatory T (Treg) cells as a distinct, highly suppressive population of Treg cells that mediate wound healing. These Treg cells were enriched in intestinal lamina propria, particularly in Crohn's disease. CD161+ Treg cells had an all-trans retinoic acid (ATRA)-regulated gene signature, and CD161 expression on Treg cells was induced by ATRA, which directly regulated the CD161 gene. CD161 was co-stimulatory, and ligation with the T cell antigen receptor induced cytokines that accelerated the wound healing of intestinal epithelial cells. We identified a transcription-factor network, including BACH2, RORγt, FOSL2, AP-1 and RUNX1, that controlled expression of the wound-healing program, and found a CD161+ Treg cell signature in Crohn's disease mucosa associated with reduced inflammation. These findings identify CD161+ Treg cells as a population involved in controlling the balance between inflammation and epithelial barrier healing in the gut.Entities:
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Year: 2018 PMID： 30397350 PMCID： PMC6474659 DOI： 10.1038/s41590-018-0230-z
Source DB: PubMed Journal: Nat Immunol ISSN： 1529-2908 Impact factor: 25.606