脂肪肝疾病 (SLD) 是全球范围内肝硬化和终末期肝癌的主要原因，影响着全球近四分之一的人口。 SLD包括代谢功能障碍相关的酒精性肝病（MetALD）和代谢功能障碍相关的脂肪变性肝病（MASLD），导致无症状的肝脏脂肪变性、纤维化、肝硬化和相关并发症。免疫过程包括肠道菌群失调、脂肪-肝脏器官串扰、肝细胞死亡和免疫细胞介导的炎症过程。值得注意的是，各种免疫细胞，如 B 细胞、浆细胞、树突状细胞、常规 CD4 和 CD8 T 细胞、先天性 T 细胞、血小板、中性粒细胞和巨噬细胞在 MetALD 和 MASLD 的发展中发挥着至关重要的作用。针对肝细胞死亡、炎症反应和肠道微生物群的免疫调节包括 N-乙酰半胱氨酸、selonsertib、F-652、泼尼松、己酮可可碱、阿那白滞素、JKB-121、HA35、奥贝胆酸、益生菌、益生元、抗生素和 FMT。了解 SLD 的免疫学机制对于推进临床治疗策略至关重要。

Steatotic liver diseases (SLD) are the principal worldwide cause of cirrhosis and end-stage liver cancer, affecting nearly a quarter of the global population. SLD includes metabolic dysfunction-associated alcoholic liver disease (MetALD) and metabolic dysfunction-associated steatotic liver disease (MASLD), resulting in asymptomatic liver steatosis, fibrosis, cirrhosis and associated complications. The immune processes include gut dysbiosis, adipose-liver organ crosstalk, hepatocyte death and immune cell-mediated inflammatory processes. Notably, various immune cells such as B cells, plasma cells, dendritic cells, conventional CD4+ and CD8+ T cells, innate-like T cells, platelets, neutrophils and macrophages play vital roles in the development of MetALD and MASLD. Immunological modulations targeting hepatocyte death, inflammatory reactions and gut microbiome include N-acetylcysteine, selonsertib, F-652, prednisone, pentoxifylline, anakinra, JKB-121, HA35, obeticholic acid, probiotics, prebiotics, antibiotics and FMT. Understanding the immunological mechanisms underlying in SLD is crucial for advancing clinical therapeutic strategies.