IL33 and asthma: The consequences are twofold and endotype-defining: IL-1β drives neutrophilic inflammation and Th17 responses, characteristic of Th2-low asthma, while IL-18 potently synergizes with IL-33 to hyperactivate group 2 innate lymphoid cells (ILC2s), exacerbating eosinophilic inflammation in Th2-high asthma (74, 75).