IL5 and allergic disease: Experimentally, ILC2 can be activated readily after allergen exposure by a single exposure to proteolytic allergens (e.g., Alternaria species) [23] and can also be stimulated chronically by epithelial activation (through direct injury or activation of pattern-recognition receptors) and subsequent production of epithelium-derived cytokines in association with environmental exposure to pollutants, irritants, fungi, and viruses, thereby producing IL-5 and IL-13, causing lung eosinophilia and AHR regardless of atopy/allergy [8].