Inflammation mediated by adipose tissue (AT) resident immune cells is a major driver of insulin resistance and type 2 diabetes (T2D). Maintaining the balance between anti- and pro-inflammatory immune cells is crucial for the prevention of adipose tissue inflammation. This balance however is tipped in favour of pro-inflammatory cells under obese conditions. A specialised population of regulatory T (Treg) cells that reside in the adipose tissue counteracts inflammation and preserves insulin resistance. This Treg cell population declines during obesity, which leads to the exacerbation of inflammation in adipose tissue. We discovered that AT Treg cells specifically required the cytokine IL-33 for their differentiation and maintenance. IL-33 led to the expansion of Treg cells specifically in the AT and reverted insulin resistance when administered to obese mice. TCR signalling induced transcription factor IRF4 contributed to Treg cell IL-33 sensing by regulating the expression of IL-33 receptor ST2. Furthermore, I will discuss how novel physiological signals regulate IL-33 signalling to facilitate differentiation and maintenance of AT Treg cells.