Summary

Excess energy intake and a sedentary lifestyle have led to increasing incidence of obesity which is a major risk factor for the development of insulin resistance. Research in the last two decades has revealed that chronic-low grade inflammation in adipose tissue is a key link between obesity and insulin resistance. As a result, adipose tissue is now considered an active immune organ with a key role in metabolic homeostasis. In the course of obesity, cells of the immune system infiltrate visceral adipose tissue (VAT) in an active process that promotes local and systemic inflammation. This inflammatory process in VAT is driven by various subsets of immune cells and is a central mechanism connecting obesity with its metabolic complications. One key event of adipose tissue inflammation is the switching of macrophages towards a pro-inflammatory phenotype. In addition, recent research has discovered an expanding list of immune cells contributing to this inflammatory process. Pro-inflammatory immune cells are crucial to obese VAT inflammation because of their production of cytokines, which can interfere with insulin signaling in peripheral tissues. This review summarizes our current knowledge of the pathology of innate and adaptive immune cells in obese adipose tissue, with emphasis in the immunological mechanisms mediating obesity-associated insulin resistance.