Autoimmune hepatitis is a necroinflammatory process of liver, featuring interface hepatitis by T cells, macrophages and plasma cells that invade to periportal parenchyma. In this process, a variety of cytokines are secreted and liver tissues undergo fibrogenesis, resulting in the apoptosis of hepatocytes. Autophagy is a complementary mechanism for restraining intracellular pathogens to which the innate immune system does not provide efficient endocytosis. Hepatocytes with their particular regenerative features are normally in a quiescent state, and, autophagy controls the accumulation of excess products, therefore the liver serves as a basic model for the study of autophagy. Impairment of autophagy in the liver causes the accumulation of damaged organelles, misfolded proteins and exceeded lipids in hepatocytes as seen in metabolic diseases. In this review, we introduce autoimmune hepatitis in association with autophagy signaling. We also discuss some genes and proteins of autophagy, their regulatory roles in the activation of hepatic stellate cells and the importance of lipophagy and tyrosine kinase in hepatic fibrogenesis. In order to provide a comprehensive overview of the regulatory role of autophagy in autoimmune hepatitis, the pathway analysis of autophagy in autoimmune hepatitis is also included in this article.

自身免疫性肝炎是肝脏的一种坏死性炎症过程，其特征在于界面病毒由侵入门静脉周围实质的T细胞，巨噬细胞和浆细胞侵袭。在此过程中，多种细胞因子被分泌，肝组织发生纤维化，从而导致肝细胞凋亡。自噬是一种抑制细胞内病原体的补充机制，而先天免疫系统无法提供有效的内吞作用。具有特定再生特征的肝细胞通常处于静止状态，并且自噬可控制多余产物的积累，因此肝脏可作为自噬研究的基本模型。肝脏中自噬的受损会导致受损细胞器的积累，错误折叠的蛋白质以及肝细胞中脂质的过量代谢，如在代谢性疾病中所见。在这篇综述中，我们介绍了自体免疫信号传导与自身免疫性肝炎。我们还讨论了自噬的一些基因和蛋白，它们在肝星状细胞激活中的调控作用以及脂肪吞噬和酪氨酸激酶在肝纤维化中的重要性。为了提供自噬在自身免疫性肝炎中的调节作用的全面概述，本文还包括自噬在自身免疫性肝炎中的途径分析。