Fig. 2

Activating and inhibitory effects of other innate and adaptive immune cell types within the hepatocellular carcinoma microenvironment. In contrast to cDCs and mregDCs, anti-inflammatory pDCs can result in the exhaustion phenotype of CTLs through various mechanisms. PMN-MDSCs and T_regs also have direct inhibitory effects on the cytotoxic function of CTLs. T_H17 cells, M-MDSCs and MAIT cells are also indirectly involved in the dysfunction phenotype of CTLs. NK cells are known antitumor protagonists through their cytotoxic activity; hence, HCC-ME inhibits the cytotoxic properties of NK cells. NKT cells are another type of lymphoid cell that exhibit antitumor functions. TME tumor microenvironment, HCC hepatocellular carcinoma, CTLs cytotoxic T lymphocytes, cDCs conventional dendritic cells, pDCs plasmacytoid dendritic cells, mregDCs mature DCs enriched in immunoregulatory molecules, M-MDSCs monocytic myeloid-derived suppressor cells, PMN-MDSCs polymorphonuclear myeloid-derived suppressor cells, NK natural killer, NKT cells natural killer T, MAIT mucosal-associated invariant T, IL interleukin, TGF transformant growth factor, IFN-γ interferon-γ, TNF tumor necrosis factor, TNFR TNF receptor, HSCs hepatic stellate cells, IRF interferon regulatory factor, NR4A1 nuclear stellate cells-4A1, TM4SF1 transmembrane-4 L six family member-1, TDEs tumor-derived exosomes, circUHRF1 circular ubiquitin-like with PHD and ring finger domain-1, CXCL C-X-C motif ligand, cGAS cyclic GMP-AMP, STING stimulator of interferon genes, TCR T-cell receptor, ARG arginase, ROS reactive oxygen species