An inducible circular RNA circKcnt2 inhibits ILC3 activation to facilitate colitis resolution

Benyu Liu, Buqing Ye, Xiaoxiao Zhu, Liuliu Yang, Huimu Li, Nian Liu, Pingping Zhu, Tiankun Lu, Luyun He, Yong Tian () and Zusen Fan ()
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Benyu Liu: Chinese Academy of Sciences
Buqing Ye: Chinese Academy of Sciences
Xiaoxiao Zhu: Chinese Academy of Sciences
Liuliu Yang: Chinese Academy of Sciences
Huimu Li: Chinese Academy of Sciences
Nian Liu: Chinese Academy of Sciences
Pingping Zhu: Chinese Academy of Sciences
Tiankun Lu: Chinese Academy of Sciences
Luyun He: Chinese Academy of Sciences
Yong Tian: Chinese Academy of Sciences
Zusen Fan: Chinese Academy of Sciences

Nature Communications, 2020, vol. 11, issue 1, 1-14

Abstract: Abstract Group 3 innate lymphoid cells (ILC3) are an important regulator for immunity, inflammation and tissue homeostasis in the intestine, but how ILC3 activation is regulated remains elusive. Here we identify a new circular RNA (circRNA) circKcnt2 that is induced in ILC3s during intestinal inflammation. Deletion of circKcnt2 causes gut ILC3 activation and severe colitis in mice. Mechanistically, circKcnt2, as a nuclear circRNA, recruits the nucleosome remodeling deacetylase (NuRD) complex onto Batf promoter to inhibit Batf expression; this in turn suppresses Il17 expression and thereby ILC3 inactivation to promote innate colitis resolution. Furthermore, Mbd3−/−Rag1−/− and circKcnt2−/−Rag1−/− mice develop severe innate colitis following dextran sodium sulfate (DSS) treatments, while simultaneous deletion of Batf promotes colitis resolution. In summary, our data support a function of the circRNA circKcnt2 in regulating ILC3 inactivation and resolution of innate colitis.

Date: 2020
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DOI: 10.1038/s41467-020-17944-5

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