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. 2022 Jul 19;12:931995. doi: 10.3389/fonc.2022.931995

Figure 1.

Figure 1

Innate immune response in HCC-BM. In HCC pathogenesis, hepatic stellate cells (HSCs) drive fibrogenesis by promoting extracellular matrix (ECM), as well as directly influencing proliferation by expressing pro-inflammatory cytokines like interleukin-6 (IL-6) and hepatocyte growth factor (HGF). HSCs also express the glycoprotein CD44v3 that promotes cell migration and invasion in HCC. Natural killer T (NKT) cells also promote fibrogenesis while neutrophils express vascular endothelial growth factor (VEGF) to promote angiogenesis and proliferation. Neutrophils also activate monocytes that can both repress HCC by expressing interferon-gamma (IFN-γ) and promote HCC by expressing interleukin-10 (IL-10). Kupffer cells (KCs) also play a crucial role in HCC pathogenesis by promoting monocytes by expressing C-C motive chemokine ligand-2 (CCL2), which acts as a monocyte attracting protein. KCs also express damage-associated molecular pattern molecules (DAMPs) and are activated by HSC. Expression of histamine (HA) and epidermal growth factor (EGF), as well as HCC expression of reactive oxygen species (ROS) and hepatocyte growth factor (HGF). However, KC expression is modulated by myeloid-derived suppressor cells (MDSCs).