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Single-cell analysis of chromatin accessibility in the human intestine identifies regulatory programs and clarifies genetic associations in Crohn’s disease

Yu Ning Zhao, Ran Zhou, Zepeng Mu, Peter Carbonetto, Xiaoyuan Zhong, Bingqing Xie, Kaixuan Luo, Zhiwei Jiang, Jianqiao Liu, Candace M. Cham, koval jason, Xin He, Andrew Dahl, Xuanyao Liu, Eugene B. Chang, Anindita Basu, Sebastian Pott

Peer-reviewed journal

In the authors' words

Crohn's disease is a complex inflammatory bowel disease resulting from an interplay of genetic, microbial and environmental factors. Cell-type-specific contributions to Crohn's disease etiology and genetic risk are incompletely understood. Here we built a comprehensive atlas of cell-type-resolved chromatin accessibility comprising 557,310 candidate cis-regulatory elements (cCREs) in terminal ileum and ascending colon from 23 patients with active and inactive Crohn's disease and 16 healthy controls. We identified cell-type-specific, anatomical location-specific and context-specific cCREs and characterized the regulatory programs underlying inflammatory responses in the intestinal mucosa of patients with Crohn's disease. These cell-type-resolved data confirmed that Crohn's disease heritability is primarily enriched in adaptive immune cells, in particular T cells, and in innate immune cells, including neutrophils. Using fine-mapped, noncoding Crohn's disease variants, we identified 30 variants located within cCREs. Our atlas provides a comprehensive resource to study gene-regulatory effects in Crohn's disease and health and highlights the cellular complexity underlying Crohn's disease risk.

Main resultThe abstract does not state a limitation.

Appeared: Sunday, September 27. Nature Genetics. Peer-reviewed journal.

DOI: 10.1038/s41588-026-02755-z