EVs from CCl4-treated hepatocytes drive a positive feedback loop between HSC and T cells involving a TLR3-IL-17A axis that enhances liver fibrosis [53], while EVs from free fatty acid- or lysolecithin-treated hepatocytes stimulate chemotaxis and pro-inflammatory molecule production by macrophages [17,18], endothelial cell tube formation and angiogenesis [23], and HSC activation [22,54]. Here, TLR3 is linked to Hepatic fibrosis.