It is now broadly accepted that white adipose tissue disorders, such as obesity, are associated with a chronic low-grade inflammation predisposing to the development of insulin-resistance, type 2 diabetes and cardiovascular complications. In obesity, accumulation of visceral adipose tissue, rather than subcutaneous adipose tissue, is regarded as the most critical factor contributing to the pathogenesis of these metabolic diseases. Recently has emerged the notion that inflammatory response accompanying obesity corresponds to a cytokine-mediated activation of innate immunity. The purpose of this review is to provide an update on this emerging concept and to show the reader how innate immune metabolic pathways engaged within white adipose tissue could interfere with innate inflammatory immune defense. First, adipose tissue is reported as an important in vivo source of inflammatory cytokines and adipocytes express some receptors of the innate immune system (namely the Toll-like receptors). Second, both innate and adaptive immune cells (respectively, macrophages, dendritic-like cells and T-lymphocytes) appear more and more essential to the initiation and the development of adipose tissue inflammation. More specifically, adipose tissue macrophages have recently emerged as key players in the inflammatory process of obese adipose tissue. Their number and their phenotypic switch from a non inflammatory (i.e. M2) to an inflammatory (i.e. M1) state are likely crucial in the onset of obese adipose tissue inflammation and in the development of insulin-resistance. Finally, the hormonal regulation of adipose tissue inflammation is exemplified by recent data regarding the role of glucocorticoids, both at the level of adipose cells and macrophages. Altogether, adipose tissue might therefore be regarded as a true immune organ, at the crossroad between metabolism and immune system.