Table 4.
Liver disease | Exacerbating | Protective |
---|---|---|
NASH | - Increased activation and apoptosis of KCs - Increased recruitment of MoMFs - Increased production of pro-inflammatory (IL-1β, TNF-α, IL-6, IL-8 MCP-1) or pro-fibrogenic (TGF-β, PDGF-β) factors - Increased recruitment of other immune cells - Orchestrating immune response to PAMPs and DAMPs |
- Removal of apoptotic, necrotic or senescent cells - Clearance of translocating from the gut bacteria |
ALD | - Increased activation and apoptosis of KCs - Increased recruitment of MoMFs - Increased production of pro-inflammatory (IL-1β, TNF-α, IL-6, IL-8 MCP-1) or pro-fibrogenic (TGF-β, PDGF-β) factors - Increased recruitment of other immune cells - Orchestrating immune response to PAMPs and DAMPs |
- Removal of apoptotic, necrotic or senescent cells - Clearance of translocating from the gut bacteria |
Viral hepatitis | - Increased activation of KCs - Decreased expression and responsiveness of TLR2 and TLR3 in cells infected with HCV - Increased IL-10 and decreased IL-1β production in cells infected with HBV leading to immune tolerance |
- Orchestrating recruitment and immune response from NK and NKT cells to limit infection |
AIH | - Activation and necroptosis of KCs - Increased production of pro-inflammatory factors |
- No data available |
Toxic injury | - Increased activation and apoptosis of KCs - Increased recruitment of MoMFs - Increased production of pro-inflammatory factors (IL-1β, TNF-α, IL-6, IL-8 MCP-1) - Increased expression of immunosuppressive PD-L1 |
- Removal of apoptotic and necrotic cells |
Liver fibrosis | - Increased activation and apoptosis of KCs - Increased recruitment of MoMFs - Increased production of pro-fibrogenic TGF-β and PDGF-β |
- Production of MMP-9, -12 and -13 supporting fibrosis resolution |
Liver cancer | - Increased production of pro-inflammatory factors creating pro-tumorigenic environment TAMs and MDSCs: - Increased production of IL-10 and expression of PD-L1 limiting cancer recognition by T cells - Increased production of TGF-β and PDGF-β promoting tumor proliferation and neoangiogenesis |
- Clearance of hepatocytes that underwent oncogene-induced senescence at early stages |