Research examines IL-33's role in asthma pathophysiology, highlighting its implications for treatment strategies.
Extract Interest in the role of interleukin (IL)-33 in asthma was sparked by genome-wide association studies linking IL-33 genetic variants with blood eosinophil counts and different asthma phenotypes [1, 2]. Both coding and non-coding IL-33 variants have been associated with protection from or risk for asthma [3, 4], but the exact mechanisms linking IL-33 with airway inflammation and hyperreactivity remain elusive. The discovery that IL-33, a member of the IL-1 cytokine family, was a ligand for IL-1R1 (ST2) and induced cytokine gene expression from T helper 2 (Th2) cells was a major advance [5].
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Georas et al. (2026) studied this question.
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