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Immunological mechanisms in the pathophysiology of non-alcoholic steatohepatitis.

Vonghia L, Michielsen P, Francque S - Int J Mol Sci (2013)

Bottom Line: Non-alcoholic steatohepatitis (NASH) is characterized by the presence of steatosis, inflammation and hepatocyte injury and constitutes hepatic manifestation of the metabolic syndrome.Obesity is considered a chronic low-grade inflammatory state and the liver has been recognized as being an "immunological organ".This review focuses on the disturbances of the cells constituting the innate and adaptive immune system in the liver and in adipose tissue.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology and Hepatology, University Hospital Antwerp, Wilrijkstraat 10, Edegem 2650, Belgium. lvonghia@gmail.com.

ABSTRACT
Non-alcoholic steatohepatitis (NASH) is characterized by the presence of steatosis, inflammation and hepatocyte injury and constitutes hepatic manifestation of the metabolic syndrome. The pathogenesis of NASH is complex and implicates cross-talk between different metabolically active sites, such as liver and adipose tissue. Obesity is considered a chronic low-grade inflammatory state and the liver has been recognized as being an "immunological organ". The complex role of the immune system in the pathogenesis of NASH is currently raising great interest, also in view of the possible therapeutic potential of immunotherapy in NASH. This review focuses on the disturbances of the cells constituting the innate and adaptive immune system in the liver and in adipose tissue.

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Related in: MedlinePlus

Overview of the immune pathways implicated in the pathogenesis of non-alcoholic steatohepatitis (NASH). DC: dendritic cells; Treg: T regulatory cell; NKT: natural killer T cells; NEU: neutrophil; MONO: monocyte; HEPA: hepatocyte; HSC: hepatic stellate cell; MF: myofibroblast; KC: Kupffer cell; EO: eosinophil; T: T lympohcyte; B: B lymphocyte; M: macrophage; CLS: crown like stucture; OPN: osteopontin; Shh: sonic hedgehog; LPS: lipopolysaccaride; FFA: free fatty acids; IP-10: interferon γ-induced protein-10; MCP-1: monocyte chemotactic protein-1; MMP-2: matrix metalloproteinase-2; MPO: myeloperoxidase; TLR: toll-like receptor; STAT3: signal transducer and activator of transcription 3; IL: interleukin. Blue lightning bolts indicate stimulation and red lightning bolts indicate inhibition. See text for details.
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f1-ijms-14-19867: Overview of the immune pathways implicated in the pathogenesis of non-alcoholic steatohepatitis (NASH). DC: dendritic cells; Treg: T regulatory cell; NKT: natural killer T cells; NEU: neutrophil; MONO: monocyte; HEPA: hepatocyte; HSC: hepatic stellate cell; MF: myofibroblast; KC: Kupffer cell; EO: eosinophil; T: T lympohcyte; B: B lymphocyte; M: macrophage; CLS: crown like stucture; OPN: osteopontin; Shh: sonic hedgehog; LPS: lipopolysaccaride; FFA: free fatty acids; IP-10: interferon γ-induced protein-10; MCP-1: monocyte chemotactic protein-1; MMP-2: matrix metalloproteinase-2; MPO: myeloperoxidase; TLR: toll-like receptor; STAT3: signal transducer and activator of transcription 3; IL: interleukin. Blue lightning bolts indicate stimulation and red lightning bolts indicate inhibition. See text for details.

Mentions: Many efforts have been undertaken to understand the role of the immune system in the pathogenesis of NASH, also in view of its potential therapeutic relevance. This review will focus on the disturbances of the cells constituting the innate and adaptive immune system in the liver and in the adipose tissue in NASH (Figure 1).


Immunological mechanisms in the pathophysiology of non-alcoholic steatohepatitis.

Vonghia L, Michielsen P, Francque S - Int J Mol Sci (2013)

Overview of the immune pathways implicated in the pathogenesis of non-alcoholic steatohepatitis (NASH). DC: dendritic cells; Treg: T regulatory cell; NKT: natural killer T cells; NEU: neutrophil; MONO: monocyte; HEPA: hepatocyte; HSC: hepatic stellate cell; MF: myofibroblast; KC: Kupffer cell; EO: eosinophil; T: T lympohcyte; B: B lymphocyte; M: macrophage; CLS: crown like stucture; OPN: osteopontin; Shh: sonic hedgehog; LPS: lipopolysaccaride; FFA: free fatty acids; IP-10: interferon γ-induced protein-10; MCP-1: monocyte chemotactic protein-1; MMP-2: matrix metalloproteinase-2; MPO: myeloperoxidase; TLR: toll-like receptor; STAT3: signal transducer and activator of transcription 3; IL: interleukin. Blue lightning bolts indicate stimulation and red lightning bolts indicate inhibition. See text for details.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3821591&req=5

f1-ijms-14-19867: Overview of the immune pathways implicated in the pathogenesis of non-alcoholic steatohepatitis (NASH). DC: dendritic cells; Treg: T regulatory cell; NKT: natural killer T cells; NEU: neutrophil; MONO: monocyte; HEPA: hepatocyte; HSC: hepatic stellate cell; MF: myofibroblast; KC: Kupffer cell; EO: eosinophil; T: T lympohcyte; B: B lymphocyte; M: macrophage; CLS: crown like stucture; OPN: osteopontin; Shh: sonic hedgehog; LPS: lipopolysaccaride; FFA: free fatty acids; IP-10: interferon γ-induced protein-10; MCP-1: monocyte chemotactic protein-1; MMP-2: matrix metalloproteinase-2; MPO: myeloperoxidase; TLR: toll-like receptor; STAT3: signal transducer and activator of transcription 3; IL: interleukin. Blue lightning bolts indicate stimulation and red lightning bolts indicate inhibition. See text for details.
Mentions: Many efforts have been undertaken to understand the role of the immune system in the pathogenesis of NASH, also in view of its potential therapeutic relevance. This review will focus on the disturbances of the cells constituting the innate and adaptive immune system in the liver and in the adipose tissue in NASH (Figure 1).

Bottom Line: Non-alcoholic steatohepatitis (NASH) is characterized by the presence of steatosis, inflammation and hepatocyte injury and constitutes hepatic manifestation of the metabolic syndrome.Obesity is considered a chronic low-grade inflammatory state and the liver has been recognized as being an "immunological organ".This review focuses on the disturbances of the cells constituting the innate and adaptive immune system in the liver and in adipose tissue.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology and Hepatology, University Hospital Antwerp, Wilrijkstraat 10, Edegem 2650, Belgium. lvonghia@gmail.com.

ABSTRACT
Non-alcoholic steatohepatitis (NASH) is characterized by the presence of steatosis, inflammation and hepatocyte injury and constitutes hepatic manifestation of the metabolic syndrome. The pathogenesis of NASH is complex and implicates cross-talk between different metabolically active sites, such as liver and adipose tissue. Obesity is considered a chronic low-grade inflammatory state and the liver has been recognized as being an "immunological organ". The complex role of the immune system in the pathogenesis of NASH is currently raising great interest, also in view of the possible therapeutic potential of immunotherapy in NASH. This review focuses on the disturbances of the cells constituting the innate and adaptive immune system in the liver and in adipose tissue.

Show MeSH
Related in: MedlinePlus