It has been suggested that IL-33 can be released during necrosis in response to infection or trauma, and subsequently functions as an “alarmin.”2, 3 Pulmonary IL-33 expression is elevated with individuals with asthma, which correlates with asthma severity.4, 5 Modulation of the IL-33–ST2 axis in murine models of allergic airway disease has supported a prominent role for this cytokine in asthma.6, 7, 8, 9, 10, 11, 12 Genetic analysis also has linked polymorphisms in human IL-33–ST2 to the incidence of asthma.13 This evidence concerns the gene IL33 and infection.