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Review
. 2016 Jun;16(3):147-58.
doi: 10.4110/in.2016.16.3.147. Epub 2016 Jun 17.

The Immune Landscape in Nonalcoholic Steatohepatitis

Sowmya Narayanan  1 , Fionna A Surette  2 , Young S Hahn  1
Affiliations
Free PMC article
Review

The Immune Landscape in Nonalcoholic Steatohepatitis

Sowmya Narayanan et al. Immune Netw. 2016 Jun.
Free PMC article

Abstract

The liver lies at the intersection of multiple metabolic pathways and consequently plays a central role in lipid metabolism. Pathological disturbances in hepatic lipid metabolism are characteristic of chronic metabolic diseases, such as obesity-mediated insulin resistance, which can result in nonalcoholic fatty liver disease (NAFLD). Tissue damage induced in NAFLD activates and recruits liver-resident and non-resident immune cells, resulting in nonalcoholic steatohepatitis (NASH). Importantly, NASH is associated with an increased risk of significant clinical sequelae such as cirrhosis, cardiovascular diseases, and malignancies. In this review, we describe the immunopathogenesis of NASH by defining the known functions of immune cells in the progression and resolution of disease.

Keywords: Fatty liver; Immunity; Liver.

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Conflict of interest statement

CONFLICTS OF INTEREST: The authors declare that there are no conflicts of interest.

Figures

Figure 1
Figure 1
Immunopathogenesis of nonalcoholic steatohepatitis (NASH). Interactions between immune cells and steatotic hepatocytes or HSCs in NASH can exacerbate or ameliorate disease. DCs, dendritic cells; IL: interleukin; TNF, tumor necrosis factor; DAMPs, damage associated molecular patterns; IFN, interferon; NK cell, natural killer cell; NKT, natural killer T cell HSC, hepatic stellate cell; MPO, myeloperoxidase; ROS, reactive oxygen species.
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