Table 2.

Summary of the impairment of myeloid-derived cells in NAFLD and ALD.

	NAFLD	ALD
Monocytes	- Differentiation into tissue resident macrophages - Differentiation in DC	- Differentiation into tissue resident macrophages - Differentiation in DC
Macrophages/KC	- M1 enhancement - Imbalance of lipogenesis - Increased LPS/TLR4-mediated signaling - Increased TNF-α, IL-1β, IFN-γ, IL-6 - Fibrosis stimulation	- M1 enhancement - Increased LPS/TLR4-mediated signaling - Increased TNF-α, IL-1β, ROS
DC	- Altered CD8/CD4 ratio - Decreased Treg infiltration - Increased inflammation	- Increased cytokine secretion via TLRs - Increased TNF-α, IFN-γ
Neutrophils	- Liver infiltration - Progression to steatohepatitis (MPO)	- Liver infiltration - Increased TNF-α
Eosinophils	- Increased Th2-type cytokines - Increased M2 polarization	- Increased Th2-type cytokines - Increased M2 polarization

NAFLD, Non-alcoholic liver disease; ALD, alcoholic liver disease; DC, dendritic cells; IFN, interferon; IL, interleukin; KC, Kupffer cells; LPS, lipopolysaccharide; NAFLD, non-alcoholic fatty liver disease; ROS, reactive oxygen species; Th2, T helper 2; TLR, Toll-like receptor; TNF, tumor necrosis factor; Treg, T regulatory cell; MPO, myeloperoxidase.