Non-alcoholic fatty liver disease-related hepatocellular carcinoma: Is there a role for immunotherapy?

Figure 1 Immune mechanisms in nonalcoholic fatty liver disease-related hepatocellular carcinoma pathogenesis. Studies using human specimens and mouse models have shown that activated non-alcoholic steatohepatitis-associated, programmed cell death protein 1 + CD8 T cells can cause non-specific cell death of hepatocytes and promote hepatocellular carcinoma development. T helper 17 cell-derived interleukin-17, immunoglobulin A-producing cells promote non-alcoholic steatohepatitis-derived hepatocellular carcinoma development, while an overall loss of CD4 T cells may increase tumor burden size. Bregs are abundant in hepatocellular carcinoma and promote disease progression, but are not specific to nonalcoholic fatty liver disease-related hepatocellular carcinoma. The role of tumor associated macrophages in the progression of nonalcoholic fatty liver disease-related hepatocellular carcinoma is unclear. Figure created in the Mind the Graph platform, available at www.mindthegraph.com. Th: T helper; PD-1: Programmed cell death protein 1; IL: Interleukin; Bregs: Regulatory B cells; IgA: Immunoglobulin A; CXCR6: C-X-C Motif Chemokine Receptor 6; TAM: Tumor associated macrophages.