Impact of medicaid waivers on medication for opioid use disorders in residential facilities: Evidence from twenty-five states.

The global prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) is rising annually, with an incidence of approximately 30% in the adult population. Metabolic dysfunction-associated steatohepatitis (MASH), the severe form of MASLD, is featured by not only steatosis but also hepatocyte damage and inflammation. MASH progression leads to liver fibrosis, which is marked by excessive deposition of extracellular matrix produced by activated hepatic stellate cells (HSCs). Elucidating the mechanisms underlying MASLD and MASH and their progression to fibrosis, along with the discovery of effective intervention strategies, remains a critical priority in this field. The aberrant activation of immune cells has been shown to promote MASLD/MASH development. Given that the spleen is a secondary lymphoid organ harboring various immune cells, and that splenic outflow constitutes a substantial portion of intrahepatic blood flow, the potential spleen–liver axis may be important in the pathogenesis and progression of MASLD/MASH. A variety of spleen-derived immune cells, cytokines and metabolic factors have been demonstrated to link the spleen and liver. However, whether the cross-talk between the spleen and liver contributes to the progression from MASLD/MASH to fibrosis remains poorly understood. Immune cells, particularly CD8 T cells and their subsets, have garnered much attention in the pathogenesis of MASLD/MASH. Liver-resident CXCR6CD8 T cells accumulate during MASH and exhibit auto-aggressive liver damage properties. Hepatic CD8 T cells with memory phenotype have been shown to suppress fibrosis by inducing the apoptosis of activated HSCs. These reports indicate that various subsets of CD8 T cells with distinct properties may participate in MASLD/MASH development, but it remains unclear whether splenic CD8 T cells are reprogrammed during MASLD/MASH.