Abstract
Adipose tissue is a metabolic organ that plays a central role in controlling systemic energy homeostasis. Compelling evidence indicates that immune system is closely linked to healthy physiologic functions and pathologic dysfunction of adipose tissue. In obesity, the accumulation of pro-inflammatory responses in adipose tissue subsequently leads to dysfunction of adipose tissue as well as whole body energy homeostasis. Simultaneously, adipose tissue also activates anti-inflammatory responses in an effort to reduce the unfavorable effects of pro-inflammation. Notably, the interplay between adipocytes and resident invariant natural killer T (iNKT) cells is a major component of defensive mechanisms of adipose tissue. iNKT cells are leukocytes that recognize lipids loaded on CD1d as antigens, whereas most other immune cells are activated by peptide antigens. In adipose tissue, adipocytes directly interact with iNKT cells by presenting lipid antigens and stimulate iNKT cell activation to alleviate pro-inflammation. In this review, we provide an overview of the molecular and cellular determinants of obesity-induced adipose tissue inflammation. Specifically, we focus on the roles of iNKT cell-adipocyte interaction in maintaining adipose tissue homeostasis as well as the consequent modulation in systemic energy metabolism. We also briefly discuss future research directions regarding the interplay between adipocytes and adipose iNKT cells in adipose tissue inflammation.
Highlights
White adipose tissue (WAT) is a central controller of lipid and glucose homeostasis that communicates locally and with distant tissues
WAT simultaneously increases the release of anti-inflammatory cytokines, including IL-4, IL-10, and IL-2 to counteract the unfavorable effects of inflammation, WAT immunity eventually shifts toward an inflammatory state, leading to prolonged inflammation in obesity [8, 9, 13]
Recent reports from several groups including ours have shown that invariant natural killer T (iNKT)-cell-deficient mouse models (Jα18−/− and CD1d−/− mice, which are deficient in iNKT cells and both iNKT cells and type II NKT cell, respectively) are more susceptible to obesity, adipose tissue inflammation, as well as insulin resistance on a high-fat diet regimen [26, 34]
Summary
White adipose tissue (WAT) is a central controller of lipid and glucose homeostasis that communicates locally and with distant tissues. The roles of this interplay in obesity and metabolic diseases have been suggested by the findings that the immune program is intimately linked to physiological and pathological changes in WAT [6,7,8,9]. Along with enhanced WAT expansion, obesity induces both quantitative and qualitative changes in WAT immunity, which potentiates the dysfunction of adipose tissue as well as systemic energy homeostasis [10,11,12]. We emphasize the roles of the interaction between iNKT cells and adipocytes in maintaining WAT homeostasis as well as whole body energy metabolism
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