Animal Models Correlating Immune Cells for the Development of NAFLD/NASH

Abstract

This review mainly elaborates on the animal models available for understanding the pathogenesis of the second hit of non-alcoholic fatty liver disease (NAFLD) involving immune system. This is known to be a step forward from simple steatosis caused during the first hit, which leads to the stage of inflammation followed by more serious liver conditions like non-alcoholic steatohepatitis (NASH) and cirrhosis. Immune-deficient animal models serve as an important tool for understanding the role of a specific cell type or a cytokine in the progression of NAFLD. These animal models can be used in combination with the already available animal models of NAFLD, including dietary models, as well as genetically modified mouse models. Advancements in molecular biological techniques enabled researchers to produce several new animal models for the study of NAFLD, including knockin, generalized knockout, and tissue-specific knockout mice. Development of NASH/NAFLD in various animal models having compromised immune system is discussed in this review.

Keywords: APPs, acute-phase proteins; BAFF, B cell activating factor; Btk, Bruton's tyrosine kinase gene; DAMPs, damage-associated molecular patterns; HCC, hepatocellular carcinoma; IRFs, Interferon regulatory factors; JNK, c-Jun N-terminal kinase; MCD, methionine choline-deficient; NAFLD; NAFLD, non-alcoholic fatty liver disease; NASH, non-alcoholic steatohepatitis; NLRs, Nod-like receptors; PAMPs, pathogen-associated molecular patterns; immune cells; mouse models.