Key result
The balance between Th17 and Treg immune responses, along with adipokines, plays a crucial role in the progression of non-alcoholic fatty liver disease to non-alcoholic steatohepatitis.
Understanding the Th17/Treg balance and adipokine signaling in NAFLD could help identify biomarkers for disease progression and potential therapeutic targets for NASH.
May support cytokine-targeted approaches in NAFLD; leaves open need for prospective validation before practice change.
Non-alcoholic fatty liver disease (NAFLD) is a chronic progressive liver disease, coupled with metabolic syndrome, which may progress to non-alcoholic steatohepatitis (NASH). Diabetes, obesity, hypertension, hypercholesterolemia, and hypertriglyceridemia are considered to be the most common causes leading to the incidence of NAFLD. It is assumed that the accumulation of lipid deposits in hepatocytes leads to production of proinflammatory cytokines that triggers the development of liver inflammation. Regulatory T cells (Tregs) play a critical role in regulating inflammatory processes in NASH, while T helper type 17 (Th17) might functionally oppose Treg-mediated responses. In addition, important mediators of hepatic steatosis are fatty hormones known as adipokines. We aimed to describe the significance and interaction between Treg and Th17-related cytokines as well as adipokines in pathogenesis and its potential use as biomarkers of NAFLD, especially with respect to progression to NASH.
No takes yet. Share an insight, caveat, or question.
Świderska et al. (2017) conducted a review in Non-alcoholic fatty liver disease (NAFLD). Th17, Treg cells, and adipokines was evaluated. The balance between Th17 and Treg immune responses, along with adipokines, plays a crucial role in the progression of non-alcoholic fatty liver disease to non-alcoholic steatohepatitis.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: