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Adipose tissue contains various types of immunocompetent cells, and these cells of innate and adaptive immunity control adipose tissue inflammation that blunts insulin sensitivity. Recent studies have shown that adipocytes express CD1d and present lipid antigen(s) to activate natural killer T (NKT) cells. The function of adipocytes is in turn modulated by cytokines that NKT cells produce to alter the expression of anti-inflammatory adipokine(s) and the production of inflammatory and chemoattractant cytokines. These in vitro studies imply that the interaction between adipocytes and NKT cells might affect the development of not only obesity but also obesity-related diseases. To test the importance of the interaction between NKT cells and adipocytes, we examined whether an adipocyte-specific CD1d deletion affected the development of obesity, which had been demonstrated with B6.CD1d−/− (CD1d KO). We found that the interaction is indeed important to induce adipose tissue inflammation and insulin resistance in response to lipid excess. In this commentary, the advances and controversies on NKT cells and obesity are discussed based on our recent report that NKT cells play a pivotal role in the regulation of adipose tissue by communicating with adipocytes via CD1d.

Evaluation of: Lynch L, Nowak M, Varghese B et al. Adipose tissue invariant NKT cells protect against diet-induced obesity and metabolic disorder through regulatory cytokine production. Immunity 37(3), 574–587 (2012). Recent studies have revealed that not only macrophages but also T lymphocytes play active roles in the development of obesity in either an aggravating or ameliorating direction. NKT cells, a subset of innate T lymphocytes, recognize lipid antigens in the context of a nonpolymorphic MHC class I-like molecule, CD1d, implying that NKT cells are likely to participate in the process. Lynch et al. demonstrated that obese patients showed reduced NKT cell count and the reduction of body fat through therapeutic intervention induced the recovery of NKT cells. They attempted to test whether the manipulation of NKT cells (deficiency and stimulation with ligands, among others) could affect adiposity in vivo and demonstrated that NKT cells did indeed play ameliorating roles in the development of obesity, ...

8-Quinolyl esters of benzenepolycarboxylic acids form flexible molecular clefts composed of convergent quinolyl groups. 1,4-Disubstituted diquinolyl terephthalate, but not monosubstituted quinolyl benzoate, in CDCl3 extracts succinic acid and forms a two-point hydrogen-bonded complex with 1,4-dihydroxybenzene. 1,3,5-Trisubstituted triquinolyl trimesate in CDCL3-DMSO-d 6 (97/3) forms one-point, two-point, and three-point hydrogen-bonded adducts with phenol (K ≅ 1 and –ΔG ≅ 0), 1,3-dihydroxybenzene (K = 24 and –ΔG 0 = 2.2), and 1,3,5-trihydroxybenzene (K = 120M−1 and –ΔG 0 = 3.3kcal/mol at 298 K), respectively. 1,3-Disubstituted diquinolyl isophthalate forms two-point adducts of similar stability with both 1,3-dihydroxy- (K = 12) and 1,3,5-trihydroxybenzene (K = 13). These results suggests that the present molecular-clefts having otherwise flexible ester linkages readily undergo induced-fit adjustment to multifunctional guest structures and the selectivity arises from the structural complementarity...