Obesity is a primary risk factor for the development of non-alcoholic fatty liver disease
(NAFLD). NAFLD, the most common chronic liver disease in the world, represents a spectrum of disorders
that range from steatosis (NAFL) to steatohepatitis (NASH) to cirrhosis. It is anticipated that
NAFLD will soon surpass chronic hepatitis C infection as the leading cause for needing liver transplantation.
Despite its clinical and public health significance no specific therapies are available. Although
the etiology of NAFLD is multifactorial and remains largely enigmatic, it is well accepted that
inflammation is a central component of NAFLD pathogenesis. Despite the significance, critical immune
mediators, loci of immune activation, the immune signaling pathways and the mechanism(s) underlying disease
progression remain incompletely understood. Recent findings have focused on the role of Interleukin 17 (IL-17) family of
proinflammatory cytokines in obesity and pathogenesis of obesity-associated sequelae. Notably, obesity favors a Th17
bias and is associated with increased IL-17A expression in both humans and mice. Further, in mice, IL-17 axis has been
implicated in regulation of both obesity and NAFLD pathogenesis. However, despite these recent advances several important
questions require further evaluation including: the relevant cellular source of IL-17A production; the critical IL-
17RA-expressing cell type; the critical liver infiltrating immune cells; and the underlying cellular effector mechanisms.
Addressing these questions may aid in the identification and development of novel therapeutic targets for prevention of inflammation-
driven NAFLD progression.