الفهرس 
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Abstract
NAFLD is the condition of liver lipid accumulation, resembling alcohol-induced injury but occurring in patients who do not use alcohol or maximum 2-3 glasses/day.
Potential steps involved in the pathogenesis of NAFLD include abnormalities of lipid metabolism, production of reactive oxygen species, increased hepatic lipid peroxidation, activated stellate cells, and abnormal patterns of cytokine production. According to the multihit theory, the first hit involves accumulation of fat in the hepatic parenchyma, probably due to insulin resistance commonly observed in patients with NAFLD. Later, leptin has been involved in the pathogenesis of NAFLD.
NKT cells are a unique subset of T lymphocytes found in mice, humans, and other mammals. Like NK cells, they exhibit features of innate immunity, but they also share properties with conventional T lymphocytes.
Depletion of NKT cells promotes proinflammatory polarization of hepatic cytokine production that sensitizes the liver to LPS toxicity, and elevation of hepatic NKT cells by adoptive transfer improved NAFLD.