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PURPOSE OF REVIEW: Asthma is a heterogeneous disease encompassing distinct phenotypes and endotypes. Advances in elucidating the pathogenic role of type 2 (T2) cytokines and epithelial-derived alarmins have profoundly reshaped our understanding of airway inflammation in asthma. This review provides an updated perspective on how these mediators contribute to asthma pathobiology and examines their integration into emerging precision medicine strategies. RECENT FINDINGS: Biologic agents targeting T2 cytokines (IL-4, IL-5, and IL-13) and alarmins (TSLP and IL-33) have demonstrated efficacy across a broad spectrum of severe asthma phenotypes. Recent evidence underscores the central role of alarmins in orchestrating both innate and adaptive immune responses within the airways. In parallel, the development of alarmin-associated molecular and clinical biomarkers is expanding patient stratification beyond traditional eosinophilic and allergic profiles. SUMMARY: Advancing our understanding of alarmins and T2 cytokines offers new opportunities to refine asthma endotyping, personalize therapeutic decisions, and pursue sustained disease remission. Future directions include the integration of multiomics, real-world evidence, and novel biomarker platforms to consolidate the next phase of precision medicine in asthma and optimize long-term disease modification strategies.
Poto et al. (Wed,) studied this question.