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000181533 037__ $$aDKFZ-2022-02065
000181533 041__ $$aEnglish
000181533 082__ $$a610
000181533 1001_ $$aPeiseler, Moritz$$b0
000181533 245__ $$aImmune mechanisms linking metabolic injury to inflammation and fibrosis in fatty liver disease - novel insights into cellular communication circuits.
000181533 260__ $$a[S.l.]$$bWiley-Blackwell$$c2022
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000181533 500__ $$a2022 Oct;77(4):1136-1160 / #DKFZ-MOST-Ca197#
000181533 520__ $$aNon-alcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease and is emerging as the leading cause of cirrhosis, liver transplantation and hepatocellular carcinoma (HCC). NAFLD is a metabolic disease that is considered the hepatic manifestation of the metabolic syndrome; however, during the evolution of NAFLD from steatosis to non-alcoholic steatohepatitis (NASH), to more advanced stages of NASH with liver fibrosis, the immune system plays an integral role. Triggers for inflammation are rooted in hepatic (lipid overload, lipotoxicity, oxidative stress) and extrahepatic (gut-liver axis, adipose tissue, skeletal muscle) systems, resulting in unique immune-mediated pathomechanisms in NAFLD. In recent years, the implementation of single-cell RNA-sequencing and high dimensional multi-omics (proteogenomics, lipidomics) and spatial transcriptomics have tremendously advanced our understanding of the complex heterogeneity of various liver immune cell subsets in health and disease. In NAFLD, several emerging inflammatory mechanisms have been uncovered, including profound macrophage heterogeneity, auto-aggressive T cells, the role of unconventional T cells and platelet-immune cell interactions, potentially yielding novel therapeutics. In this review, we will highlight the recent discoveries related to inflammation in NAFLD, discuss the role of immune cell subsets during the different stages of the disease (including disease regression) and integrate the multiple systems driving inflammation. We propose a refined concept by which the immune system contributes to all stages of NAFLD and discuss open scientific questions arising from this paradigm shift that need to be unravelled in the coming years. Finally, we discuss novel therapeutic approaches to target the multiple triggers of inflammation, including combination therapy via nuclear receptors (FXR agonists, PPAR agonists).
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000181533 650_7 $$2Other$$aFXR agonists
000181533 650_7 $$2Other$$aHCC
000181533 650_7 $$2Other$$aKupffer cells
000181533 650_7 $$2Other$$aMAFLD
000181533 650_7 $$2Other$$aNAFLD
000181533 650_7 $$2Other$$aNASH
000181533 650_7 $$2Other$$aPPAR agonists
000181533 650_7 $$2Other$$aSingle-cell sequencing
000181533 650_7 $$2Other$$acancer immunotherapy
000181533 650_7 $$2Other$$aexhausted T cells
000181533 650_7 $$2Other$$aimmune-mediated liver disease
000181533 650_7 $$2Other$$amacrophages
000181533 650_7 $$2Other$$ascRNA-seq
000181533 650_7 $$2Other$$aspatial transcriptomics
000181533 7001_ $$aSchwabe, Robert$$b1
000181533 7001_ $$aHampe, Jochen$$b2
000181533 7001_ $$aKubes, Paul$$b3
000181533 7001_ $$0P:(DE-He78)66ed2d4ec9bc11d29b87ac006adf85e5$$aHeikenwälder, Mathias$$b4$$udkfz
000181533 7001_ $$aTacke, Frank$$b5
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