Western lifestyle, characterized by increased consumption of energy-dense foods and little physical activity, is leading to an increasingly common incidence of obesity and diabetes. Although obesity is one of the greatest public health burdens, there are still unanswered questions about the exact mechanisms that contribute to the development of obesity-related metabolic disorders. In this context, adipocyte enlargement, along with dysfunctional immune cells, plays a critical role in obesity pathogenesis, gradually leading to low grade systemic inflammation. Recent data suggest that a group of innate immune cells residing in the adipose tissue, termed group 2 innate lymphoid cells (ILC2), may play an important role in maintaining metabolic health. ILC2, through the production of the type 2 cytokines IL-5 and IL-13, promote the function of eosinophils and tissue-resident macrophages to maintain white adipose tissue (WAT) function. Interestingly, obese mice display a significant reduction in WAT ILC2, which enhances the progression of metabolic inflammation. However, how obesity impacts ILC2 is still poorly understood. Our previous work shows that dietary cues control the function of ILC2 by altering their cellular metabolism. In this project, we aim to investigate the effects of a high-fat diet on ILC2 metabolism in WAT and how ILC2-intrinsic metabolic changes modulate the progression of metaflammation. Overall, our project aims to elucidate the immunological and metabolic mechanisms underlying obesity-related inflammation and to develop novel therapeutics to combat obesity, one of the major challenges in the industrialized world.