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. 2022 Nov 30;13:1029085. doi: 10.3389/fimmu.2022.1029085

Table 4.

Effects of disease on tissue-resident macrophages in the liver.

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