Abstract
Hepatic stellate cells (HSCs) are strategically located to interact with hepatocytes, sinusoidal endothelial and Kupffer cells, and hepatic resident and migratory cells of the immune system. Compelling evidence in recent years has demonstrated that HSCs recruit inflammatory and immune cells by producing specific cytokines and chemokines. Upon activation or appropriate stimulation, HSCs express or upregulate MHC class I and II and co-regulatory B7 family molecules (e.g., CD80, CD86, and B7-H1), but suppress activation/proliferation of conventional CD4+ and CD8+ T cells and cause their apoptosis. Paradoxically, HSCs induce expansion of regulatory CD4+CD25+FoxP3+ T cells (Tregs). Whereas HSC-expanded Tregs acquire greater immunosuppressive potential, HSC-modulated dendritic cells become poor stimulators of T-cell activation. These characteristics of HSCs are likely critical in the liver’s inherent tolerogenicity and potentially important in liver allograft tolerance. On the other hand, HSCs can present bacterial lipid antigens to natural killer T cells and play an important role in limiting bacterial infection.
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