Asthma is a heterogeneous disease characterized by various endotypes, which are defined by distinct molecular mechanisms.
The primary endotypes of asthma are Type 2-high (T2-high) and Type 2-low (T2-low).
T2-high asthma is characterized by elevated levels of type 2 cytokines IL-4, IL-5, and IL-13.
T2-high asthma endotype is often associated with eosinophilic inflammation and includes both allergic and non-allergic asthma.
Patients with T2-high asthma typically respond well to corticosteroids and targeted biologic therapies.
Targeted therapies include as anti-IL-5 (mepolizumab, reslizumab), anti-IL-4/IL-13 (dupilumab), and anti-IgE (omalizumab).
T2-low asthma is a more heterogeneous group, that includes neutrophilic and paucigranulocytic asthma.
This endotype is less well-defined and often associated with Th1 and Th17 pathways, involving cytokines such as IL-17 and TNF-α.
T2-low asthma is typically less responsive to corticosteroids and may require alternative treatments.
T2-high asthma can be further divided into early-onset allergic asthma and late-onset eosinophilic asthma, while T2-low asthma includes subtypes such as neutrophilic asthma and obesity-related asthma.
Understanding these endotypes allows for the selection of appropriate biologic therapies and other targeted interventions based on the underlying pathophysiology of the disease.