Abstract
Nonalcoholic fatty liver disease (NAFLD) is a condition characterized by hepatic accumulation of excess lipids. T cells are commonly classified into various subsets based on their surface markers including T cell receptors, type of antigen presentation and pathophysiological functions. Several studies have implicated various T cell subsets and natural killer (NK) cells in the progression of NAFLD. While NK cells are mainly components of the innate hepatic immune system, the majority of T cell subsets can be part of both the adaptive and innate systems. Several studies have reported that various stages of NAFLD are accompanied by the accumulation of distinct T cell subsets and NK cells with different functions and phenotypes observed usually resulting in proinflammatory effects. More importantly, the overall stimulation of the intrahepatic T cell subsets is directly influenced by the homeostasis of the gut microbiota. Similarly, NK cells have been found to accumulate in the liver in response to pathogens and tumors. In this review, we discussed the nature and pathophysiological roles of T cell subsets including γδ T cells, NKT cells, Mucosal-associated invariant T (MAIT) cells as well as NK cells in NAFLD.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is a liver impairment characterized by the presence of excessive hepatic fat accumulation caused by factors mainly related to a high fat diet
We describe the nature of T cell subsets and natural killer (NK) cells, as well as discuss their roles in the pathogenesis mechanisms of NAFLD
During the earlier development of NAFLD which is mainly characterized by simple steatosis, these cells secrete chemotaxis stimulating molecules, such as C-C motif ligand 2 (CCL2) which results in hepatic accumulation of macrophages originating from circulating monocytes [15,16]
Summary
Non-alcoholic fatty liver disease (NAFLD) is a liver impairment characterized by the presence of excessive hepatic fat accumulation caused by factors mainly related to a high fat diet. Its progression comprises a wide spectrum, ranging from simple hepatic steatosis to fibrosis and in extreme cases extending up to hepatocellular carcinoma (HCC) It comes with all manifestations and complications in liver impairment and is one of the major diseases with a global prevalence rate of 25% [5]. In. NAFLD, a variety of innate and adaptive immune cells including Kupffer cells, neutrophils, Tcells and natural killer (NK) cells have been indicated to be involved in the progression of hepatic steatosis, inflammation, and fibrosis associated [8–10]. NAFLD, a variety of innate and adaptive immune cells including Kupffer cells, neutrophils, Tcells and natural killer (NK) cells have been indicated to be involved in the progression of hepatic steatosis, inflammation, and fibrosis associated [8–10] These complex repertoires of non-parenchymal cells originating from both the lymphoid and non-lymphoid sources play key roles in hepatic immunoregulation and defense mechanisms. We describe the nature of T cell subsets and NK cells, as well as discuss their roles in the pathogenesis mechanisms of NAFLD comprising the gut-liver axis
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