Four stages of T2 asthma inflammation induction are shown. In the first stage, airborne allergens induce inflammation in lung airways through their unique properties. The best-characterized effect of allergens occurs in phase 2, in which the damaged airway epithelium releases alarmins, such as thymic stromal lymphopoietin (TSLP) and IL-33. These factors act on sentinel antigen-presenting cells, in particular local dendritic cells (DCs). During phase 3, DCs carry allergens to lung draining lymph nodes (LNs) and prime naive allergen-specific CD4⁺ T cells. Early IL-4 and other signals, many remaining undefined, promote effector Th2 differentiation and group 2 follicular Th (Tfh2 and Tfh13) cells. Tfh cells remain in the LN and promote B cell activation and the production of allergen-specific IgE and other isotypes. In phase 4, effector Th2 cells home back to the lung and, along with innate lymphoid type 2 cells (ILC2s) and lung epithelial cells, produce type 2 cytokines and CCR3 ligands, including CCL11/eotaxin-1, CCL24/eotaxin-2, CCL26/eotaxin-3, monocyte chemoattractant protein-4, and CCL5/RANTES. These cytokines and chemokines promote endothelial and epithelial activation, goblet cell hyperplasia and mucus production, mast cell (MC) and basophil (Baso) activation, and production and recruitment of eosinophils (Eos) to the lung. Approved drugs now target several of these pathways.