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.
Georas et al. (2026) studied this question.