Table 1.

Contribution of specific liver cells in the development of inflammation associated with NASH.

Type of cell	Roles in steatohepatitis	References
Hepatocytes	- sense PAMPs DAMPs, metabolite molecules (saturated FFA), and release inflammatory mediators (TNFα, IL1β) - hepatocyte death (lytic cell death > apoptosis) contribute to DAMPs induced inflammation - hepatocyte extracellular vesicles signals to immune cells	(31, 40, 41)
LSECs	- orchestrate release of proinflammatory mediators (cytokines chemokines such as MCP1, IL1/6, TNFα), (adhesion molecules such as VCAM1, ICAM) - enhance liver inflammation, injury, and fibrosis	(36, 42)
Resident and recruited macrophages	- sense PAMPs DAMPs and metabolites (saturated FFA), - contribute to the recruitment and activation of other hepatic immune cells via inflammatory chemokines and cytokines - specific subsets of liver macrophages enhance NAFLD progression	(32, 43)
NK cells/ILC1	- production of IFNγ and TNFα - regulate macrophage polarization towards a pro-inflammatory phenotype - display an anti-fibrogenic role	(24, 43, 44)
Neutrophils	- secretion of elastase, NETS - contribute to the onset of the early stage of NAFLD - promote hepatocyte injury	(45, 46)