Department of Clinical Pathobiochemistry, Faculty of Medicine, Technische Universität Dresden, MTZ, Fiedlerstrasse 42, 01307, Dresden, Germany.
Section of Metabolic Vascular Medicine, Medical Clinic III, Faculty of Medicine, TU Dresden, Dresden, Germany.
Rev Endocr Metab Disord. 2016 Mar;17(1):29-39. doi: 10.1007/s11154-016-9339-2.
The low grade inflammatory state present in obesity promotes the progression of Non-Alcoholic Fatty Liver Disease (NAFLD). In Non-Alcoholic Steatohepatitis (NASH), augmented hepatic steatosis is accompanied by aberrant intrahepatic inflammation and exacerbated hepatocellular injury. NASH is an important disorder and can lead to fibrosis, cirrhosis and even neoplasia. The pathology of NASH involves a complex network of mechanisms, including increased infiltration of different subsets of immune cells, such as monocytes, T-lymphocytes and neutrophils, to the liver, as well as activation and in situ expansion of liver resident cells such as Kupffer cells or stellate cells. In this review, we summarize recent advances regarding understanding the role of the various cells of the innate and adaptive immunity in NASH development and progression, and discuss possible future therapeutic options and tools to interfere with disease progression.
肥胖症中存在的低度炎症状态会促进非酒精性脂肪性肝病(NAFLD)的进展。在非酒精性脂肪性肝炎(NASH)中,肝脂肪变性加剧伴随着异常的肝内炎症和加重的肝细胞损伤。NASH 是一种重要的疾病,可导致纤维化、肝硬化,甚至肿瘤。NASH 的病理学涉及一个复杂的机制网络,包括不同免疫细胞亚群(如单核细胞、T 淋巴细胞和中性粒细胞)向肝脏的浸润增加,以及肝脏固有细胞(如枯否细胞或星状细胞)的激活和原位扩增。在这篇综述中,我们总结了关于理解先天和适应性免疫的各种细胞在 NASH 发展和进展中的作用的最新进展,并讨论了可能的未来治疗选择和干预疾病进展的工具。