Review demonstrates that targeting bile acid metabolites regulates Th17 and Treg balance in primary biliary cholangitis, suggesting new therapeutic targets.
Primary biliary cholangitis (PBC) is a prototypical autoimmune hepatobiliary disease that is pathologically characterized by persistent cholestasis and selective obliteration of the interlobular bile ducts. T helper cell 17 (Th17) and regulatory T cells (Treg) are critically implicated in the immunopathogenesis of PBC. Accumulated bile acid metabolites, such as isoalloLCA, in patients with PBC modulate the differentiation and functional dynamics of Tregs and Th17 cells. Notably, disruption of the Th17/Treg balance in PBC exacerbates biliary inflammation, accelerates the deterioration of hepatic fibrosis, and increases the likelihood of evolving hepatocellular carcinoma (HCC). Recent advances in targeting the bile acid metabolites to control the Th17/Treg balance have unveiled novel therapeutic avenues. Pharmacological agents have demonstrated efficacy in maintaining the Th17/Treg rebalance, showing significant therapeutic promise for PBC. This review provides new insights into the treatment of PBC by systematically summarizing the central role of bile acid metabolites in the differentiation of Th17 and Treg cells and investigating the feasibility of related targeted therapies.
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Liu et al. (2025) studied this question.
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