原发性硬化性胆管炎（PSC）常伴发溃疡性结肠炎（UC），合并率高达80%。PSC合并UC（PSC-UC）具有不同于单纯UC的疾病特点，好发于右半结肠且癌变率极高；然而，其发病机制并不明确。固有淋巴样细胞（ILCs）是一类黏膜特异性定植的免疫细胞，其组成和功能的改变与肠黏膜稳态的维持和肠道炎症的发生密切相关。PSC疾病过程中，显著变化的肠道胆汁酸总量和其合成/代谢中间产物成分改变可能是PSC-UC肠道炎症的重要因素，而该过程离不开胆汁酸受体的介导。在前期研究中，通过人和小鼠ILCs单细胞转录组学分析，我们发现ILCs细胞仅对一种胆汁酸受体高表达，即LXR-β。基于此，我们推测胆汁酸及其相关中间产物可能通过LXR-β的介导，直接调控ILCs组成和功能，并在PSC-UC的发病过程中发挥重要作用。

Primary sclerosing cholangitis (PSC) is often accompanied by ulcerative colitis (UC), with a combined rate of up to 80%. PSC combined with UC (PSC-UC) has different disease characteristics from UC alone. It occurs in the right colon and has a high carcinogenic rate; however, its pathogenesis is currently unclear. Innate lymphoid cells (ILCs) are a type of mucosal-specific colonized immune cells. The changes in composition and function are closely related to the maintenance of intestinal mucosal homeostasis and intestinal inflammation. In the course of PSC disease, significant changes in the amount and composition of intestinal bile acids may be important factors for intestinal inflammation of PSC-UC, and this process cannot be separated from the function of bile acid receptors. In previous studies, single cell RNAseq (scRNAseq) were performed for analyzing transcriptomics of human and mouse ILCs and found that ILCs cells overexpressed only one bile acid receptor, LXR-β. Based on these evidences, we speculate that bile acid and its related intermediates may directly regulate the composition and function of ILCs through LXR-β, and play an important role in the pathogenesis of PSC-UC.