engleski

The role of immune mechanisms in development of metabolic syndrome in obesity

More than billion of obese and overweight people live currently in the world. A significant number of them develop diabetes mellitus type 2 (DM2) and non-alcoholic fatty liver disease (NAFLD). Mechanisms that induce inflammation and trigger transition from prediabetes to DM2 or from hepatic steatosis to non-alcoholic steatohepatitis (NASH) are still unclear. In this research I found that γδ T cells are enriched in visceral adipose tissue and they produce proinflammatory cytokines. In response to high fat diet (HFD), there is increase in number of γδ T cells that produce IL-17A. Research on NAFLD revealed that initiating event, in response to high calorie diet, is the increase in expression of the NKG2D ligand H60 on hepatocytes. Upregulation of ligands leads to mobilisation of γδ T cells through an NKG2D engagement that induces an increase in IL-17A. Lack of either γδ T cells, NKG2D or IL-17A significantly decreases development of liver fibrosis.

diabetes mellitus type 2 ; γδ T cells ; IL-17A ; non-alcoholic fatty liver disease ; NKG2D receptor ; stress induced molecules

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