Immunomodulatory properties of UDCA have been controversially discussed in the past [259] [260] [261] [262] . The glucocorticoid receptor in rat hepatocytes is activated by UDCA in a ligand-independent way, whereas suppression of IFN-γinduced MHC class II expression was found to be glucocorticoid-receptor-dependent [263] . It remains to be defined whether glucocorticoid receptor activation is unique to UDCA, and thus therapeutically relevant, or might be shared by endogenous bile salts.