Published: 2 July 2024
Author(s): Ningning Mi, Qiangsheng He, Yuyao Liu, Yingmei Li, Ying Li, Yingjie Wu, Man Yang, Yingya Zhao, Peng Xie, Wenjing Li, Siqin Wu, Zijun Li, Danni Wang, Xiwen Qin, Jinqiu Yuan, Pingguang Lei, Jian Qi, Bin Xia
Section: Original Article

Inflammatory bowel disease (IBD), encompassing Crohn's disease (CD) and ulcerative colitis (UC), is a chronic inflammatory disease of the gastrointestinal tract driven by an inappropriate and continuing inflammatory response in a genetically susceptible host [1]. Early evidence from twin studies showed that the concordance rate in monozygotic twins with CD and UC was 30–35 % and 10–15 %, respectively, supporting a role for genetics in the risk of IBD [1]. Recent advancements in our understanding of IBD have identified specific genes and genetic loci associated with susceptibility, quantified by polygenic risk scores (PRS) [2,3]

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