TABLE 1

Airway diseases driven by type 2 inflammation [17–24, 26–41]

	Evidence of type 2 inflammation	Proportion of type 2 patients	Comorbid disease prevalence
Asthma
Uncontrolled asthma despite medium- to high-dose ICS	Elevated serum IgE Elevated serum eosinophils	51%	+ CRSwNP 30–50% + Allergic rhinitis >80% + COPD [33] ∼13% + NSAID-ERD/AERD ∼7%
Severe asthma	Elevated sputum eosinophils Expression of IL-13-inducible genes and Th2 genes in sputum cells	55–70%
Difficult asthma despite high-dose ICS	Elevated blood eosinophils or F_eNO	71%
CRSwNP	Elevated CLC and IL-13 gene expression Elevated IL-5 and Th2 gene expression	∼80%	+ Asthma 50% + Allergic rhinitis ∼75% + NSAID-ERD/AERD ∼10–20%
COPD	Persistent blood eosinophils ≥300 cells·µL⁻¹ or ≥2%	15–37%	A subset may also present with asthma [33] + Allergic rhinitis ∼7% + CRS [42, 43]
Allergic rhinitis	IgE-mediated disease driven by type 2 inflammation [10, 37, 38]	100%	Comorbid asthma [37] 19–38% Comorbid CRS [38] ∼67%

ICS: inhaled corticosteroids; CRSwNP: chronic rhinosinusitis with nasal polyps; NSAID-ERD: nonsteroidal anti-inflammatory drug-exacerbated respiratory disease; AERD: aspirin-exacerbated respiratory disease; IL: interleukin; Th2: type 2 T-helper; F_eNO: exhaled nitric oxide fraction; CLC: Charcot–Leyden crystals; CRS: chronic rhinosinusitis.