Separating sensitization and regulatory T-cell functions in patients with food allergy

In this issue of the Journal, Noval Rivas et al1 address this question and demonstrate the role of type 2 innate lymphoid cells (ILC2s) in this process using a previously reported mouse model of food allergy. Because of an activating mutation (Il4raF709) in the IL-4Rα chain that results in enhanced signaling through IL-4 and IL-13, the mice used in this study are prone to the development of food allergy.2 Importantly, the authors were able to use this enhanced phenotype to examine mechanisms thought to be key in the sensitization events of food allergy, particularly the IL-33/IL-33 receptor ST2 axis, through generating Il4raF709 mice that lacked expression of the IL-33 receptor ST2 (Il1rl1-/-).