Zetterman R K, Sorrell M F
Gastroenterology. 1981 Sep;81(3):616-24.
Continuing hepatic injury despite cessation of ethanol intake has suggested a potential role for altered humoral and cellular immunity in the pathogenesis of alcoholic liver disease. Variation of cell-mediated response has been observed most commonly in patients with alcoholic hepatitis. These alterations include decreased mitogen response in vitro, reduction of circulating T-cell numbers with a corresponding increase of intrahepatic T-cells, lymphokine production in vitro in response to isolated alcoholic hyalin (Mallory bodies), and in vitro evidence of increased spontaneous cell-mediated cytotoxicity. Fewer immunologic alterations are detected in patients with alcoholic fatty liver or cirrhosis. At present, these observations have not established a definite causal relationship between ethanol-induced liver injury and immunologic mechanisms. Studies utilizing in vitro correlates of cellular immunity in alcoholics are carried out after development of hepatic injury. To establish the role of humoral and cellular immune events in the pathogenesis of alcoholic liver injury will require development of a suitable animal model.
尽管停止摄入乙醇,但肝脏仍持续损伤,这表明体液免疫和细胞免疫改变在酒精性肝病发病机制中可能发挥作用。细胞介导反应的变化最常见于酒精性肝炎患者。这些改变包括体外有丝分裂原反应降低、循环T细胞数量减少及肝内T细胞相应增加、体外对分离的酒精透明小体(马洛里小体)产生淋巴因子、以及体外证据表明自发细胞介导的细胞毒性增加。酒精性脂肪肝或肝硬化患者检测到的免疫改变较少。目前,这些观察结果尚未确立乙醇诱导的肝损伤与免疫机制之间明确的因果关系。在肝脏损伤发生后,对酗酒者进行了利用细胞免疫体外相关性的研究。要确定体液免疫和细胞免疫事件在酒精性肝损伤发病机制中的作用,将需要建立合适的动物模型。