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@ARTICLE{Peiseler:181533,
      author       = {M. Peiseler and R. Schwabe and J. Hampe and P. Kubes and M.
                      Heikenwälder$^*$ and F. Tacke},
      title        = {{I}mmune mechanisms linking metabolic injury to
                      inflammation and fibrosis in fatty liver disease - novel
                      insights into cellular communication circuits.},
      journal      = {Journal of hepatology},
      volume       = {77},
      number       = {4},
      issn         = {0168-8278},
      address      = {[S.l.]},
      publisher    = {Wiley-Blackwell},
      reportid     = {DKFZ-2022-02065},
      pages        = {1136-1160},
      year         = {2022},
      note         = {2022 Oct;77(4):1136-1160 / #DKFZ-MOST-Ca197#},
      abstract     = {Non-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).},
      subtyp        = {Review Article},
      keywords     = {FXR agonists (Other) / HCC (Other) / Kupffer cells (Other)
                      / MAFLD (Other) / NAFLD (Other) / NASH (Other) / PPAR
                      agonists (Other) / Single-cell sequencing (Other) / cancer
                      immunotherapy (Other) / exhausted T cells (Other) /
                      immune-mediated liver disease (Other) / macrophages (Other)
                      / scRNA-seq (Other) / spatial transcriptomics (Other)},
      cin          = {F180},
      ddc          = {610},
      cid          = {I:(DE-He78)F180-20160331},
      pnm          = {316 - Infektionen, Entzündung und Krebs (POF4-316)},
      pid          = {G:(DE-HGF)POF4-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35750137},
      doi          = {10.1016/j.jhep.2022.06.012},
      url          = {https://inrepo02.dkfz.de/record/181533},
}