Why the study?
Current therapeutic options for NASH are limited, and understanding the role of immune cells in NASH pathogenesis should aid in designing innovative targeted drugs.
This review highlights the critical role of immune cell-mediated inflammatory processes in the progression of NAFLD to NASH, suggesting potential targets for innovative drug design.
Immune inflammation merits targeted exploration in NASH trials; leaves open validation of specific cell pathways.
Non-alcoholic fatty liver disease (NAFLD) includes a range of hepatic manifestations, starting with liver steatosis and potentially evolving towards non-alcoholic steatohepatitis (NASH), cirrhosis or even hepatocellular carcinoma. NAFLD is a major health burden, and its incidence is increasing worldwide. Although it is primarily a disease of disturbed metabolism, NAFLD involves several immune cell-mediated inflammatory processes, particularly when reaching the stage of NASH, at which point inflammation becomes integral to the progression of the disease. The hepatic immune cell landscape is diverse at steady state and it further evolves during NASH with direct consequences for disease severity. In this Review, we discuss current concepts related to the role of immune cells in the onset and progression of NASH. A better understanding of the mechanisms by which immune cells contribute to NASH pathogenesis should aid the design of innovative drugs to target NASH, for which current therapeutic options are limited.
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Huby et al. (2021) studied this question.
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