부산대학교 도서관

Objective Systemic low-grade chronic inflammation has been intensively investigated in obese subjects. Recently, various immune cell types have been implicated in the pathogenesis of adipose tissue inflammation. However, the roles of invariant natural killer T cells (iNKT cells) and the regulation of iNKT cell activity in adipose tissue are not thoroughly understood. In this study, we have revealed the dynamics of the iNKT cell population in the adipose tissue of obese subjects and the role of adipocyte CD1d molecules in iNKT cell activation as well as in adipose tissue inflammation. Methods To investigate the roles of iNKT cells in adipose tissue inflammation, we analyzed Ja18 KO mice after high fat diet feeding. In addition, we used primary adipocytes from CD1d KO mice to examine the role of adipocyte CD1d in iNKT cell activation. Results We demonstrated that iNKT cells were decreased in number in the adipose tissue of obese subjects. Interestingly, CD1d, a molecule involved in lipid antigen presentation to iNKT cells, was highly expressed in adipocytes and CD1d-expressing adipocytes stimulated iNKT cell activity through physical interaction. iNKT cell population and CD1d expression were reduced in the adipose tissue of obese mice and humans compared to those of lean subjects. Moreover, iNKT cell-deficient Ja18 knockout mice became more obese and exhibited increased adipose tissue inflammation at the early stage of obesity. Conclusion Our data suggest that adipocytes regulate iNKT cell activity via CD1d and that the interaction between adipocytes and iNKT cells may modulate adipose tissue inflammation in obesity.