Ursodeoxycholic acid impairs liver‐infiltrating T‐cell chemotaxis through IFN‐γ and CX3CL1 production in primary biliary cholangitis

Ursodeoxycholic acid (UDCA) is the primary treatment for biliary cholangitis (PBC), but its mechanism of action remains unclear. Studies suggest that UDCA enhances NF erythroid 2-related factor 2 (NFE2L2) expression and interaction between IFN-γ C-X3-C motif chemokine ligand 1 (CX3CL1) facilitates inflammation in PBC. Therefore, we examined effects on CX3CL1 vitro vivo PBC models such as human liver tissue, a murine model, cell lines, isolated intrahepatic epithelial cells (IHBECs). We observed significant decrease mRNA levels positive correlations post-UDCA livers. NFE2L2-mediated transcriptional activation was significantly enhanced UDCA-treated Jurkat cells. In 2-octynoic acid-immunized mice, production by liver-infiltrating T dependent NFE2L2 activation. dose-dependentlyinduced expression, which decreased HuCC-T1 IHBECs upon treatment. These results UDCA-induced suppression attenuates chemotactic adhesive abilities