LAUSR

The increasing prevalence of non-alcoholic fatty liver disease (NAFLD), as well as its advanced stage non-alcoholic steatohepatitis (NASH) with the progression of liver inflammation and cell death with or without hepatic fibrosis, brings a heavy burden to public health (1). Non-alcoholic fatty liver disease is commonly associated with the incidence of obesity and diabetes (2, 3). In the United States, the prevalence of obesity raised from 30.5 to 42.4% from years 1999–2000 to years 2017–2018 as the Centers for Disease Control and Prevention (CDC) reported, and the prevalence of severe obesity also increased from 4.7 to 9.2% at this period. Recently, a new nomenclature of NAFLD, metabolic associated fatty liver disease (MAFLD), was recommended, which is thought to be more accurate to reflect the clinical pathogenesis of this disease with metabolic dysfunction (4, 5). There is no appropriate treatment for NAFLD up to date, except for early prevention via change of lifestyle (2, 6). Understanding the cellular and molecular pathogenesis of NAFLD and its relative advanced liver disease is helpful to define new potential targets for treatment. Hepatic immunity plays a critical role in the pathogenesis of liver diseases (7, 8), including NAFLD, NASH, and end-stage of liver disease. Both hepatic innate and adaptive immune cells, as well as their interaction, orchestrate the progression of NAFLD and NASH (9). For example, the accumulation of activated hepatic B cells driven by gut microbiota impacted liver inflammation and fibrosis via modulating both intrahepatic innate and adaptive immunity during the progression of NASH (10). New functions of special types of T cells are reported to be associated with the progression of NAFLD and hepatocellular carcinoma (HCC) defined by the single-cell RNA sequencing (sRNA-seq) technology (11, 12). Here, we mainly focus on the latest investigation of the function of special types of T cells in NAFLD and NAFLD-related primary liver cancer.