摘要
The growing diffusion of nonalcoholic fatty liver disease(NAFLD) is a consequence of the worldwide increase in the prevalence of obesity.Oxidative stress is widely recognized to play a pivotal role in NAFLD evolution to nonalcoholic steatohepatitis(NASH).Here we review recent evidence suggesting that oxidative stress-derived antigens originating within fatty livers stimulate both humoral and cellular adaptive immune responses and the possible mechanisms involved in sustaining hepatic inflammation in NASH.
The growing diffusion of nonalcoholic fatty liver disease（NAFLD） is a consequence of the worldwide increasein the prevalence of obesity. Oxidative stress is widelyrecognized to play a pivotal role in NAFLD evolution tononalcoholic steatohepatitis （NASH）. Here we reviewrecent evidence suggesting that oxidative stress-derivedantigens originating within fatty livers stimulate bothhumoral and cellular adaptive immune responses andthe possible mechanisms involved in sustaining hepaticinflammation in NASH.
