fig1

Figure 1. Schematic mechanism of immune evasion across the spectrum from inflammation by chronic hepatitis B (HBV) and C virus (HCV) infection to resultant hepatocellular carcinoma (HCC). The complexity of the mechanism involves multiple immune cells and various collections of cytokines. A: immune tolerance induced by HBV and HCV infection; B: immune evasion driven by the crosstalk between tumour cells and immune cells in HCC. DC: dendritic cells; MDSCs: myeloid-derived suppressor cells; TAMs: tumour-associated macrophages; NK: natural killer; NKT: natural killer T; Treg: regulatory T-cells; CAF: cancer-associated fibroblast; HBV: hepatitis B virus; HCV: hepatitis C virus; MHC: major histocompatibility complex; TCR: T-cell receptor; IL: interleukin; IFNg: interferon gamma; TNFa: tumour necrosis factor receptor alpha; TGF-β: transforming growth factor beta; CCL: C-C motif chemokine ligand; CXCL: C-X-C motif ligand 1; Gal-9: galactin-9; PD-1: programmed cell death protein; PD-L1: programmed cell death ligand 1; CTLA: cytotoxic T-lymphocyte-associated protein; IL: interleukin; Arg-1: arginase-1; Tim-3: T cell immunoglobulin and mucin domain 3; LAG-3: lymphocyte-activation gene 3; SDF-1: Stromal cell-derived factor 1