Immunological mechanisms of nonalcoholic fatty liver disease Jacek Michałkiewicz, Piotr Socha Medical Science Review - Hepatologia 2009; 9 95-101 aaICID: 902251
Article type: Review article
IC™ Value: 3.04
Abstract provided by Publisher
Cellular mechanisms of nonalcoholic fatty liver disease are presented. The data are based on animal models of this syndrome, i.e. leptin-deficient ob/ob mice and leptin-resistant fa/fa rats and db/db mice. The following issues are discussed: a) the role of adipose tissue cellular composition, distribution, and products in the induction of systemic chronic inflammatory response, b) the significance of inflammatory mediators and microbial products (LPS) in the pathogenesis of NAFLD, and c) possible cellular mechanisms of NAFLD progression. In conclusion, NAFLD progression is connected with changes in the cellular composition and function of certain lymphocyte subsets in the liver bearing the CD4+ NKT phenotype. Their excess number and activity are related to a high production of profibrotic factors. Selective expansion of these cells depends on the appropriate cytokine pattern induced by pro-inflammatory mediators of adipose tissue and microbial products.