FIGURE 1.

Type‐2 airway inflammation is driven by an adaptive and innate immune response driven by epithelial alarmins (particularly IL‐33 and thymic stromal lymphopoietin). Type‐2 airway inflammation is detected in clinical practice by assessing fractional exhaled nitric oxide (reflecting airway IL‐13 activity) and blood eosinophils (reflecting systemic IL‐5 activity). The main functional consequence of type‐2 inflammation is airflow limitation as a result of airway mucus plugging, airway wall oedema and thickening, airway smooth muscle hyperplasia and the induction of airway hyperresponsiveness. Key cellular players, cytokines, chemokines, effector mediators and their receptors, are shown. Coloured crosses indicate the pathways inhibited by the relevant biologic (shown in same colour); corticosteroids inhibit most pathways at the cost of associated toxicity.