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Review
. 2013 Aug 30;7 Suppl 2(Suppl 2):771-81.
doi: 10.1007/s12072-013-9468-6. eCollection 2013 Dec.

Immune and inflammatory pathways in NASH

Michal Ganz  1 , Gyongyi Szabo  1
Affiliations
Review

Immune and inflammatory pathways in NASH

Michal Ganz et al. Hepatol Int. .

Abstract

Immune and inflammatory pathways have a central role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Both the innate and adaptive immune systems contribute to the development of NAFLD. Pathogen-associated molecular patterns and danger-associated molecular patterns are known to activate a variety of pattern-recognition receptors that result in inflammation. The key features of the immune system and inflammatory pathways in the development of NAFLD are discussed in this review.

Keywords: DAMPs; Immunity; Inflammation; NAFLD; NASH; PAMPs.

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Figures

Fig. 1
Fig. 1
Immune response in NASH. The immune response in NASH is initiated by both pathogen-associated molecular danger signals and danger-associated molecular signals. This response involves both the innate and adaptive branches of the immune system and results in inflammation
Fig. 2
Fig. 2
Pattern recognition receptors in NASH. A variety of pattern-associated molecular patterns and danger-associated molecular patterns are involved in the pathogenesis of NASH. PAMP and DAMP signaling can occur through various PRRs, including Toll-like receptors, nucleotide-binding and oligomerization domain (NOD)-like receptors, and RIG-I like receptors. PRR signaling can result in steatosis, insulin resistance, and inflammatory cell activation and recruitment
Fig. 3
Fig. 3
Cross-talk in NASH. The immune and inflammatory response in NASH involves an interaction among the liver, gut, and adipose tissue. Various adipokines, including adiponectin, interleukin-6 (IL-6), leptin, tumor necrosis factor α (TNFα), and monocyte chemoattractant protein-1 (MCP-1), are released by adipocytes and macrophages in adipose tissue and contribute to inflammation in the liver. Increased gut permeability, bacterial overgrowth, and changes in microbiota can result in the production of LPS, fatty acids, and other factors that contribute to liver inflammation and steatosis
See this image and copyright information in PMC

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