Obesity is closely related to various lifestyle-related diseases including diabetes, hypertension and atherosclerosis and is thought to be aggravated with a chronic inflammation in adipose tissue induced by immunocompetent cells such as macrophages and T cells. NKT cells are distributed as well and recognize lipid antigens. We previously reported that NKT cell-deficient, CD1d^-/- mice had less gain of body weight and maintained insulin sensitivity when compared with WT mice fed on a high fat diet.

In the present study, we examined the interactions between NKT cells and adipocytes developed from 3T3-L1 cells. 3T3-L1 cells expressed CD1d and could load a-GalCer on it to present to iNKT cells. Both iNKT cells and NKT cells from Ja18^-/- mice could be activated by 3T3-L1 cells without addition of external ligand. Since we could not detect significant level of expression of a-glycosylceramide/CD1d complex recognized by L363 antibody on 3T3-L1, an endogenous ligand other than a-GlyCer may be presented to NKT cells in the context of CD1d. Upon activation NKT cell produced IFN-g that stimulated 3T3-L1 cells to induce more CD1d expression. Furthermore, the level of adiponectin secreted by adipocytes which had an anti-inflammatory role was decreased by IFN-g treatment. Taken together, adipocytes could activate NKT cells by presenting endogenous ligand and NKT cells could modulate adipose tissue more inflammatory through an NKT cell-adipocyte interaction.