ILC2s were originally found to be activated by epithelial cell derived cytokines to induce the secretion of Th2 cytokines, IL-5 and IL-13. Recent research has shown that lipid mediators play a large role in the activation and inhibition of ILC2 function. Unlike the traditional epithelial cell derived cytokines IL-33 and IL-25, lipid mediators have been shown to promote ILC2 secretion of not only IL-5 and IL-13, but the secretion of IL-4 as well. Prostaglandin D 2 has been shown to be a potent chemoattractant of ILC2s as well as a potent activator of ILC2s to release Th2 cytokines. In addition to prostaglandin D 2 , cysteinyl leukotrienes also activate ILC2s to secrete Th2 cytokines during inflammation. Notably, lipid mediators have been shown to work in concert with epithelial cell derived cytokines to increase IL-5 and IL-13 secretion from ILC2s. On the other hand, lipid meditators prostaglandin I 2 and lipoxin A 4 are the first identified lipid mediator inhibitors of ILC2 function, and thus limit ILC2 contribution to Th2 inflammation. ILC2s play a potential significant role in Th2 mediated inflammation in a variety of allergic disease states, such as asthma, atopic dermatitis, and chronic rhinosinusitis. The identification of lipid mediators as activators and inhibitors of ILC2 function provides additional therapeutic targets for altering ILC2 function during disease states.