Schematic representation of the potential ant-inflammatory role of IL-33 in adipose tissue inflammation. Tissue damage caused by factors such as high free fatty acids, ER stress, oxidative stress, and inflammation can lead to necrosis of cells and release of biologically active IL-33. This can interact with its receptor ST2L on a number of cell types within adipose tissue (adipocytes themselves, CD4+ Th2 cells and Fat-Associated Lymphoid Cluster (FALC) cells) leading to the production of protective Th2 cytokines (e.g. IL-5, IL-10 and IL-13). IL-33 can polarize macrophages towards an alternatively activated (M2) phenotype and reduce lipid uptake in adipocytes and macrophages via the down-regulation of several metabolic genes.