Adipocyte CD1d determines adipose inflammation and insulin resistance in obesity

ABSTRACT

Obesity-induced adipose tissue inflammation is regulated by various immune cells for innate and adaptive immunity. Among adipose tissue immune cells, it has been proposed that invariant Natural Killer T (iNKT) cells play crucial roles in anti-inflammatory responses in obesity. iNKT cells recognize ‘lipid’ antigens loaded on CD1d of antigen presenting cells and modulate immune responses by secreting Th1 or Th2 type cytokines depending on species of lipid antigens, antigen presenting cell types, and environmental cytokine milieu. However, the regulatory mechanisms of antigen presenting cells for adipose iNKT cell stimulation have not been clearly elucidated. Recently, we have reported that CD1d expressing adipocytes could act as an antigen presenting cell for adipose iNKT cells by characterization of adipocyte-specific CD1d knockout (CD1d^ADKO) mice. Upon high-fat diet (HFD) feeding, CD1d^ADKO mice aggravated adipose tissue inflammation and insulin resistance compared with CD1d^f/f mice. In this commentary, we provide the additional data of adipocyte CD1d-dependent regulation of adipose iNKT cell responses as well as systemic insulin sensitivity. In addition, we discuss how the interaction between adipocytes and iNKT cells would be regulated with the progression of obesity.

KEYWORDS:

• adipocyte
• adipose tissue inflammation
• adipose tissue macrophage
• CD1d
• invariant Natural Killer T cell
• insulin sensitivity
• lipid antigen presentation
• obesity

Disclosure of potential conflicts of interest

No potential conflicts of interest were disclosed.

Acknowledgments

We are grateful to Jeu Park for critical reading of the manuscript.

Additional information

Funding

This work was supported by the National Research Foundation (NRF) funded by the Korean government (the Ministry of Science, ICT & Future Planning), [2011-0018312].