HDAC9 and metabolic dysfunction-associated steatohepatitis: SCFAs, in particular, directly promote Treg differentiation by acting as histone deacetylase (HDAC) inhibitors, enhancing IL-10 production [48,49], or migrating to bone marrow to induce tolerogenic antigen presenting cells (APCs), thereby reducing effector T cell recruitment and tissue inflammation [45], while Lactobacillus-associated bile acids like ursodeoxycholic acid (UDCA), isoDCA, and isoLCA modulate the Treg/Th17 balance in the ileum and liver, as demonstrated in nonalcoholic steatohepatitis (NASH) models [50].