Indexed on: 24 Jul '13Published on: 24 Jul '13Published in: Journal of Gastroenterology and Hepatology
Activated hepatic stellate cells (HSCs) have been considered as a major type of cells in liver fibrosis by producing a huge amount of extracellular matrix, especially collagen fibers, and profibrotic mediators such as transforming growth factor-beta, interleukin-6 and monocyte chemoattractant protein-1. Recently, accumulated evidence suggests that the liver is an immunologic organ because of enrichment of diverse types of immune cells and that their interactions with HSCs are closely related with the progression of liver fibrosis. However, the underlying mechanisms of interaction between HSCs and immune cells remain largely unknown. Recently, several studies have demonstrated that natural killer cells, M2 macrophages, regulatory T cells, and bone marrow derived CD11b(+) Gr1(+) immature cells ameliorate liver fibrosis, whereas neutrophils, M1 macrophages, CD8 T cells, natural killer T cells and interleukin-17-producing cells accelerate liver fibrosis. However, there are still controversial issues about their functions during liver fibrogenesis. In this review, we summarize the diversity roles of immune cells (e.g. profibrotic/antifibrotic or both) in regulating the activation of HSCs during hepatic fibrogenesis, in which several producible mediators by HSCs play important roles in the interaction with them. Moreover, the current cell-based therapies using immune cells against liver fibrosis are discussed.