{"doi":"10.1016/j.jcmgh.2020.06.003","title":"Nature or Nurture? The Answer Is “Both” in Nonalcoholic Steatohepatitis","abstract":"In the 4 decades since its initial description as a cause of chronic liver disease,1Ludwig J. Viggiano T.R. McGill D.B. Oh B.J. Nonalcoholic steatohepatitis: Mayo Clinic experiences with a hitherto unnamed disease.Mayo Clin Proc. 1980; 55: 434-438PubMed Google Scholar nonalcoholic steatohepatitis (NASH) has become the most common cause of chronic liver disease worldwide.2Younossi Z. Anstee Q.M. Marietti M. Hardy T. Henry L. Eslam M. George J. Bugianesi E. Global burden of NAFLD and NASH: trends, predictions, risk factors and prevention.Nat Rev Gastroenterol Hepatol. 2018; 15: 11-20Crossref PubMed Scopus (2385) Google Scholar Epidemiologically, NASH tracks with the obesity epidemic,2Younossi Z. Anstee Q.M. Marietti M. Hardy T. Henry L. Eslam M. George J. Bugianesi E. Global burden of NAFLD and NASH: trends, predictions, risk factors and prevention.Nat Rev Gastroenterol Hepatol. 2018; 15: 11-20Crossref PubMed Scopus (2385) Google Scholar which has led to the recognition that environmental exposure to an obesogenic diet plays a key role in its pathogenesis.3Carr R.M. Oranu A. Khungar V. Nonalcoholic fatty liver disease: pathophysiology and management.Gastroenterol Clin North Am. 2016; 45: 639-652Abstract Full Text Full Text PDF PubMed Scopus (140) Google Scholar,4Chalasani N. Younossi Z. Lavine J.E. Charlton M. Cusi K. Rinella M. Harrison S.A. Brunt E.M. Sanyal A.J. The diagnosis and management of nonalcoholic fatty liver disease: practice guidance from the American Association for the Study of Liver Diseases.Hepatology. 2018; 67: 328-357Crossref PubMed Scopus (3275) Google Scholar This nurture argument suggests that the majority of NASH sequelae can be explained and therefore remedied by dietary alteration. Although there is undoubtedly a dietary contributor to NASH pathogenesis, there is growing literature on how individual-specific differences contribute or compound NASH pathogenesis. Among these nature contributors is the role of the body’s immune system. In this issue of Cellular and Molecular Gastroenterology and Hepatology, Van Herck et al5Van Herck M.A. Vonghia L. Kwanten W.J. Julé Y. Vanwolleghem T. Ebo D.G. Michielsen P.P. De Man J.G. Gama L. De Winter B.Y. Francque S.M. Diet reversal and immune modulation show key role for liver and adipose tissue T cells in murine nonalcoholic steatohepatitis.Cell Mol Gastroenterol Hepatol. 2020; 10: 467-490Abstract Full Text Full Text PDF PubMed Scopus (14) Google Scholar describe in the article “Diet reversal and immune modulation show key role for liver and adipose tissue T cells in murine non-alcoholic steatohepatitis” that T-cell subpopulations are modulated in the liver and adipose tissue of mice fed a NASH-inducing diet. Van Herck et al5Van Herck M.A. Vonghia L. Kwanten W.J. Julé Y. Vanwolleghem T. Ebo D.G. Michielsen P.P. De Man J.G. Gama L. De Winter B.Y. Francque S.M. Diet reversal and immune modulation show key role for liver and adipose tissue T cells in murine nonalcoholic steatohepatitis.Cell Mol Gastroenterol Hepatol. 2020; 10: 467-490Abstract Full Text Full Text PDF PubMed Scopus (14) Google Scholar examined the fate of several T-cell populations (T helper [Th]1, Th17, regulatory T [Treg], and cytotoxic T [Tc] cells) in both liver and adipose tissue in mice fed a NASH-inducing, high-fat, high-fructose diet. In the liver, this dietary model caused hepatic steatosis, inflammation, fibrosis, and an up-regulation of key lipogenic and hepatic stellate cell activation genes. In visceral adipose tissue (VAT), the model caused adipocyte hypertrophy, inflammation, dysregulation of critical lipid regulatory genes, and increased expression of the collagen synthetic genes, Col1a1 and Col3a1. In parallel with these histologic and metabolic changes in liver and adipose tissue were profound changes in several T-cell subpopulations. Namely, the liver, VAT, and blood compartment all had increased Th17 cells. VAT had increased proportions of Tc cells and reduced Treg cells. 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