Research ArticleINFLAMMATORY BOWEL DISEASE

The orphan nuclear receptor RORα and group 3 innate lymphoid cells drive fibrosis in a mouse model of Crohn’s disease

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Science Immunology  02 Sep 2016:
Vol. 1, Issue 3, pp. eaaf8864
DOI: 10.1126/sciimmunol.aaf8864

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A check for gut fibrosis

Patients with Crohn’s disease have uncontrolled inflammation in their gut, which can lead to intestinal fibrosis and narrowing that can slow or block the movement of food. Lo et al. now report that RORα and group 3 innate lymphoid cells (ILC3) contribute to the development of fibrosis in a mouse model of Crohn’s disease. They report that mice deficient in RORα, which is involved in development of group 2 ILCs (ILC2), have diminished pathology. However, these effects are not mediated by ILC2. Instead, the authors suggest that ILC3 are critical for the development of gut fibrosis and may serve as a target for treating fibrotic complications of Crohn’s disease.