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Human retinoic acid-regulated CD161+ regulatory T cells support wound repair in intestinal mucosa

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Giovanni A M Povoleri, Estefania Nova-Lamperti, Cristiano Scottà, Giorgia Fanelli, Yun-Ching Chen, Pablo D Becker, Dominic Boardman, Benedetta Costantini, Marco Romano, Polychronis Pavlidis, Reuben McGregor, Eirini Pantazi, Daniel Chauss, Hong-Wei Sun, Han-Yu Shih, David J Cousins, Nichola Cooper, Nick Powell, Claudia Kemper, Mehdi Pirooznia & 5 more Arian Laurence, Shahram Kordasti, Majid Kazemian, Giovanna Lombardi, Behdad Afzali

Original languageEnglish
Pages (from-to)1403–1414
JournalNature Immunology
Issue number12
Early online date5 Nov 2018
Accepted/In press7 Sep 2018
E-pub ahead of print5 Nov 2018
Published1 Dec 2018


King's Authors


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.

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