Abstract
Accumulating clinical and experimental evidences have demonstrated that both innate and adaptive immunity are involved in the pathogenesis of alcoholic liver disease (ALD), in which the role of immunity is to fuel the inflammation and to drive the progression of ALD. Various immune cells are implicated in the pathogenesis of ALD. The activation of innate immune cells induced by alcohol and adaptive immune response triggered by oxidative modification of hepatic constituents facilitate the persistent hepatic inflammation. Meanwhile, the suppressed antigen-presenting capability of various innate immune cells and impaired function of T cells may consequently lead to an increased risk of infection in the patients with advanced ALD. In this review, we summarized the significant recent findings of immune cells participating in ALD. The pathways and molecules involved in the regulation of specific immune cells, and novel mediators protecting the liver from alcoholic injury via affecting these cells are particularly highlighted. This review aims to update the knowledge about immunity in the pathogenesis of ALD, which may facilitate to enhancement of currently available interventions for ALD treatment.
Highlights
Alcoholic liver disease (ALD) encompasses a broad spectrum of liver injuries ranging from steatosis with a minimal parenchymal injury to steatohepatitis, fibrosis, and cirrhosis
Chronicplus-binge ethanol feeding increased the number of hepatic type I NKT cells and induced their activation in mice, which contributes to the development of alcoholic liver injury partially by releasing inflammatory mediators that recruit neutrophils to the liver [73]
At the early stage of ALD, activation of innate immunity induced by alcohol in liver precipitates disorders ranging from localized and temporary inflammation to extensive hepatocellular damage and liver injury
Summary
Alcoholic liver disease (ALD) encompasses a broad spectrum of liver injuries ranging from steatosis with a minimal parenchymal injury to steatohepatitis, fibrosis, and cirrhosis. Chronic alcohol feeding failed to sensitize MIF−/− mice to LPS, leading to the decreased chemokine production and monocyte recruitment into the liver [29] These studies evidenced that MIF is an essential mediator in the regulation of chemokine expression and immune cell infiltration in the liver during the ethanol-induced liver injury [27,28,29]. Chronicplus-binge ethanol feeding increased the number of hepatic type I NKT cells and induced their activation in mice, which contributes to the development of alcoholic liver injury partially by releasing inflammatory mediators that recruit neutrophils to the liver [73]. The role of G-MDSCs in the chronic setting of ALD should be thoroughly elucidated, which might be a novel potential target for immune-regulatory treatment of ALD in the future
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