Abstract
Non-alcoholic fatty liver diseases (NAFLD) are liver diseases which are strongly associated with obesity. The incidence of NAFLD has been gradually increased in recent years. According to different pathology of the liver, NAFLD include three disease states: simple fatty liver, hepatitis (nonalcoholic steatohepatitis, NASH) and fatty liver cirrhosis. The accumulations of fat around the internal organs, which secrete a wide range of adipokines, such as interleukin-6, contribute the development and progress of NAFLD in obesity. In addition, the liver has been recognized as an immune organ containing several immune cells, for instance, inherited macrophages in the live (kupffer cells), nature killer cells, T lymphocytes, T regulatory cells (Tregs), myeloid-derived suppressor cells (MDSCs), and dendritic cells. These immune cells secret a number of cytokines, such as tumor necrosis factor (TNF-α) and monocyte chemoattractant protein (MCP-1), play important roles in the development of NAFLD. Moreover, a high level of fatty acids in the liver microenvironment, leads to suppress CD4(+)T cells and the loss of CD4(+)T cells in the microenvironment of the liver may be one of key factors which is associated with the progress of NAFLD to cirrhosis and liver cancer. This article aims to review the recent studies in the mechanisms of these immune cells involving in the progress of NAFLD, and to explore the novel strategies targeting these immune cells to control the prevalence of NAFLD and reduce liver fibrosis.